latest research parkinson's disease

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Parkinson's disease articles from across Nature Portfolio

Parkinson's disease is a progressive neurodegenerative disorder, which is characterized by motor symptoms such as tremor, rigidity, slowness of movement and problems with gait. Motor symptoms are often accompanied with fatigue, depression, pain and cognitive problems.

Latest Research and Reviews

Genetic and phenotypic characterization of Parkinson’s disease at the clinic-wide level

• Thomas F. Tropea
• Whitney Hartstone
• Alice S. Chen-Plotkin

Misfolded protein deposits in Parkinson’s disease and Parkinson’s disease-related cognitive impairment, a [ 11 C]PBB3 study

• Michele Matarazzo
• Alexandra Pérez-Soriano
• A. Jon Stoessl

Progression subtypes in Parkinson’s disease identified by a data-driven multi cohort analysis

• Tamara Raschka
• Holger Fröhlich

Structural underpinnings and long-term effects of resilience in Parkinson’s disease

• Verena Dzialas
• Merle C. Hoenig
• Thilo van Eimeren

Longitudinal study investigating the influence of COMT gene polymorphism on cortical thickness changes in Parkinson's disease over four years

• Amin Tajerian

Actin-nucleation promoting factor N-WASP influences alpha-synuclein condensates and pathology

• Joshua Jackson
• Christian Hoffmann
• Daniele Bano

News and Comment

Repurposing a diabetes drug to treat Parkinson’s disease

In a multicenter clinical trial, patients with early-stage Parkinson’s disease treated with lixisenatide, a drug currently used for the treatment of diabetes, showed improvement in their motor scores compared with those on placebo.

• Sonia Muliyil

Towards a methodological uniformization of environmental risk studies in Parkinson’s disease

• Bruno Lopes Santos-Lobato

Towards the era of biological biomarkers for Parkinson disease

Since its instigation in cancer research in the 1930s, the disease-staging concept has become a crucial tool in clinical research and medical practice. Two new papers have proposed biological staging and classification systems based on α-synuclein pathology for Parkinson disease and related conditions.

• Nobutaka Hattori

Parkinson disease pathology in inflammatory bowel disease

A new study has found evidence of α-synuclein aggregates — a key pathological hallmark of Parkinson disease — in the gut and brain in people and animals with inflammatory bowel disease.

• Heather Wood

Tackling vascular risk factors as a possible disease modifying intervention in Parkinson’s disease

• Anne E. Visser
• Nienke M. de Vries
• Bastiaan R. Bloem

Mapping the dysfunctome provides an avenue for targeted brain circuit therapy

Brain connections modulated by 534 deep-brain-stimulation electrodes revealed a gradient of circuits involved in dystonia, Parkinson’s disease, Tourette’s syndrome and obsessive-compulsive disorder. Together, these circuits begin to describe the human ‘dysfunctome’, a library of dysfunctional circuits that lead to various brain disorders.

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2023 Update: New Parkinson’s Disease Treatments in the Clinical Trial Pipeline

New Parkinson’s Medication on the Horizon

The development of potential new medications for Parkinson’s disease (PD) medications remains very active, with multiple new medications in various stages of research development that are aiming to treat and slow down PD.

In past blogs, we have reviewed the various mechanisms of action that are being studied to see if they result in successful slowing of disease progression.

These treatment mechanisms include:

Targeting abnormal alpha-synuclein aggregation.

• Increasing activity of GLP-1, a strategy which may block activation of immune cells in the brain
• Other strategies of decreasing inflammation in the brain
• Increasing the activity of the enzyme glucocerebrosidase to enhance the cell’s lysosomal or garbage disposal system
• Decreasing activity of the proteins LRRK2 or c-Abl to decrease neurodegeneration
• Improving function of the mitochondria – the energy-producing element of the nerve cell – to support the health of the neurons
• Increasing neurotrophic factors to enhance nerve survival
• Using cell based therapies to restore healthy nerves in the brain

Decreasing oxidative stress in the brain

Most of the compounds presented in prior blogs are continuing to be studied in various stages of clinical trials.

You can view these past blogs below:

• Neuroprotective strategies in clinical trials – 2020
• Neuroprotective strategies in clinical trials – update 2021
• Medications in clinical trials – 2022
• Therapies for non-motor symptoms in clinical trials
• Repurposed medications being studied for PD

Here are additional medications that we are keeping our eye on in 2023 and into 2024

You can read more about each of the clinical trials mentioned by following the links provided. Each is associated with an NCT number on clinicaltrials.gov,  a database of all the clinical trials for all diseases worldwide. Each link also provides the contact information for each trial if you would like to find out more about the possibility of participating in the trial.)

Decreasing activity of LRRK2

BIIB122: One compound that is successfully moving through the research pipeline is BIIB122. We previously reported on a Phase 1 study of a small molecule LRRK2 inhibitor known at the time as DNL151. The results of that study were published , and this molecule now called BIIB122, is being tested to see its efficacy in a much larger group of people.

Mutations (a change in the DNA sequence) in the LRRK2 (Leucine-rich repeat kinase 2) gene represent a common genetic cause of PD. LRRK2 plays several roles in the cell and mutations that increase its enzymatic activity are thought to cause neurodegeneration. BIIB122 is a small molecule that decreases the activity of LRRK2. The current study NCT05418673 is evaluating whether taking BIIB122 slows the progression of PD more than placebo in the early stages of PD. The study will focus on participants with specific genetic variants in their LRRK2 gene.

Butanetap : Buntanetap is a small molecule that suppresses the translation of DNA into messenger RNA of several neurotoxic proteins. This group of neurotoxic proteins produces insoluble clumps that accumulate in nerve cells, disrupting the cell’s normal function. One of these proteins is alpha-synuclein, which abnormally accumulates in PD.  In early studies, Buntanetap showed reduction of inflammation and preservation of axonal integrity and synaptic function. The current study NCT05357989 is designed tomeasure safety and efficacy of Buntanetap compared with placebo in participants with early PD.

Sulfuraphane : Sulfuraphane is an antioxidant, found in dark green vegetables such as broccoli and brussel sprouts. It is currently being studied NCT05084365 to see if it improves motor and cognitive function in PD.

Decreasing activity of the c-Abl kinase

IKT-148009 : IKT-148009 is a small molecule that decreases the activity of c-Abl, an enzyme that acts on a wide range of targets within the cell, supporting many different cellular functions. Research suggests that overactivation of c-Abl is a downstream effect of oxidative stress and may play a role in neurodegeneration in PD. There is also research to suggest that increased c-Abl activation correlates with alpha-synuclein aggregation. These findings and others led to the possibility that inhibiting c-Abl may be a helpful strategy in PD therapy. The current study NCT05424276 is investigating whether decreasing the activity of c-Abl in early, untreated people with PD is safe and tolerable, and whether it improves motor and non-motor features of the disease.

Cell-based therapy

Bemdaneprocel (BRT-DA01, previously known as MSK-DA01): A recently-completed Phase 1 study investigated the surgical transplantation of dopaminergic neuron precursor cells into the brains of people with PD. In an open label study (one without a control group) of 12 people, the treatment was found to be safe and well-tolerated. Transplantation of the cells was feasible and resulted in successful cell survival and engraftment. A phase 2 study is currently being planned for early 2024.

Decreasing inflammation

RO-7486967/selnoflast: – RO-7486967 is a small molecule that inhibits the NLRP3 inflammasome, a complex of proteins involved in inflammation that is thought to be overactive in PD. The current study NCT05924243 will investigate whether this molecule is safe and tolerable in early stages of PD.

New mechanism of action: Targeting cell death

KM819:  Apoptosis, a series of organized molecular steps that leads to programmed cell death, is a normal part of cell function.  When this system goes awry however, cells may die when they are not supposed to. KM819 is a small molecule inhibitor of Fas-associated factor1 (FAF1), a key regulator of cell death. It is being investigated to see if decreasing the process of cell death will protect neurons in PD. The current study NCT05670782 is testing this compound in both healthy adults and people with PD.

The Parkinson’s Hope List

We continue to thank Dr. Kevin McFarthing, a biochemist and person with Parkinson’s for his efforts in creating and maintaining  The Parkinson’s Hope List  — a collation of all the compounds that are being explored as new therapies for PD at all stages of the research pipeline and is updated frequently. It is an excellent source of information for those interested in the current state of PD research focused on new potential treatments. APDA was privileged to host Dr. McFarthing as a special guest on our broadcast entitled  Dr. Gilbert Hosts:Taking Research From the Lab to our Lives .

Dr. McFarthing and his colleagues put together a yearly review of the medications for Parkinson’s disease in clinical trials. The year 2023’s review can be accessed here . Dr. McFarthing and colleagues reported that as of January 2023, there were nearly 139 Parkinson’s therapies active in the clinical trial pipeline as registered on the www.clinicaltrials.gov website involving almost 17,000 participants. Of these drugs tested, 76 (55%) trials were focused on symptomatic treatment (STs), medications that attempt ameliorate the symptoms of PD; and 63 (45%) were disease-modifying therapies (DMTs), medications that attempt to slow the progression of the disease. The pipeline grew in the past year, with 35 newly registered trials (18 ST and 17 DMT trials). Most of these clinical trials (34%) are in Phase 1 (early-stage of clinical testing, primarily performed to assess for safety), while 52% have progressed to Phase 2 testing stage (mid-stage, performed in small numbers of people with PD to assess for efficacy), followed by 14% currently in Phase 3 (late-stage trials, performed in larger numbers of people with PD to assess for efficacy).

APDA proudly funds innovative work

APDA recently announced its newly-funded research grantees for the 2023-2024 academic year.  Our new pool of grantees are working on many of the strategies discussed above and will continue to push the field of PD research forward, introducing new ideas to the field and new possibilities in PD therapy.

Here are some examples:

• Dr. Nikhil Panicker is investigating the NRLP3 inflammasome. He is exploring whether reducing the activation of the inflammasome within microglia can protect neurons from accumulating alpha-synuclein in a cell model of PD.
• Dr. William Zeiger is studying the mechanisms by which the abnormal accumulation of alpha-synuclein cause thinking and memory problems in PD.
• Dr. Naemeh Pourshafie is studying the relationship between tau and alpha-synuclein, two proteins that abnormally accumulate in neurodegenerative diseases.  

We are so proud to help make this vital work possible!

Tips and takeaways

• There is hope in progress, with multiple treatment strategies in the PD research pipeline.
• Potential treatments are generally divided into two large categories: disease modifying therapies and symptomatic treatments.
• Mechanisms of action that are being studied to alter the progression of PD include: decreasing activity of LRRK2, decreasing aggregation of alpha-synuclein, decreasing oxidative stress in the brain, decreasing activity of c-Abl, introducing dopaminergic neurons into the brain, decreasing inflammation, and inhibiting programmed cell death.
• APDA supports essential research, bringing new ideas to fruition in the treatment of PD. Read more  about past work we have funded, and the projects that we are funding this year.
• We need your support in order to continue this extremely valuable research. Click  here  to make a donation.

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New therapeutic target for Parkinson’s disease discovered

• Feinberg School of Medicine

Northwestern Medicine scientists have uncovered a new mechanism by which mutations in a gene parkin contribute to familial forms of Parkinson's disease. The discovery opens a new avenue for Parkinson’s therapeutics, scientists report in a new study.

The Northwestern scientists discovered that mutations in parkin result in a breakdown of contacts between two key workers in the cell — lysosomes and mitochondria.

Mitochondria are the main producers of energy in cells, and lysosomes recycle cellular debris that accumulates during normal function of our cells. These organelles are especially important in our brains because neurons are highly dependent on energy production by mitochondria, and because of their activity, neurons produce an abundance of cellular debris that must be cleared by lysosomes.

In a prior study, published in Nature, Dr. Dimitri Krainc, chair of neurology and director of Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine, and his group discovered that lysosomes and mitochondria form contacts with each other. After the initial discovery, Northwestern scientists tried to understand the function of these contacts in Parkinson’s disease.  

In the new study published July 19 in Science Advances, the investigators report that lysosomes help mitochondria by providing key metabolites for their function. Mitochondria must import many of their essential ingredients, but it has not been well known where some of these metabolites come from. On the other hand, lysosomes serve as recycling factories in cells and, therefore, produce many breakdown products that could be used by other organelles such as mitochondria. 

In this work, scientists found that lysosomes provide important amino acids that support the function of mitochondria. However, they also found that in some forms of Parkinson’s disease, lysosomes cannot serve as a “helping hand” to mitochondria because the contacts between the two organelles are disrupted. This results in dysfunctional mitochondria and ultimately degeneration of vulnerable neurons in Parkinson’s disease.

“Findings from this study suggest that dysregulation of mitochondria-lysosome contacts contributes to the Parkinson's disease pathophysiology,” said Krainc, the study’s corresponding author. “We propose that restoring such mitochondria-lysosome contacts represents an important new therapeutic opportunity for Parkinson’s disease.”   

From a broader perspective, this study opens a new avenue of research in neurodegenerative disorders, by highlighting the importance of direct communication and collaboration between cellular organelles in the pathogenesis of these disorders.

The first author of the study is Dr. Wesley Peng who recently completed the medical scientist training program (MD-PhD) at Northwestern and currently serves as a neurology resident at Mass General Brigham and Harvard Medical School. Other contributors to the study include Leonie Schroder, Pingping Song and Yvette Wong.

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Research News

Read the latest developments, reporting and analysis from the world of Parkinson's research, including progress made in studies, tools and collaborations funded by The Michael J. Fox Foundation.

• Alpha-synuclein

What We Fund: $34.2M Toward Light Therapy for Sleep, Freezing of Gait and More

April 29, 2024

Episode 13: New Advances in Neurosurgical Interventions for Parkinson's Disease with Doris Wang

April 16, 2024

Results of Parkinson’s Trial for Diabetes Drug Lixisenatide Published

April 5, 2024

Episode 12: Accelerating Discovery by Developing and Distributing Research Tools with Nicole Polinski

April 2, 2024

A Skin Test for Parkinson’s? What You Need to Know

March 22, 2024

AD/PD 2024 Conference Highlights the Biological Era of Parkinson’s Disease

March 21, 2024

Episode 11: The Importance of Sex and Gender Factors in Neurodegenerative Disease Research and Care with Antonella Santuccione Chadha

March 19, 2024

Join the Study that's Changing Everything

The Parkinson's Progression Markers Initiative is changing how patients, families, doctors and scientists think about brain disease. Now it needs you.

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Our Foundation exists for one reason: to speed breakthroughs patients can feel in their everyday lives.

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• Immediate family member had PD
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• Extended family member or friend had PD
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New research challenges conventional picture of Parkinson's disease

by Arizona State University

Parkinson's disease, the second most common type of progressive dementia after Alzheimer's disease, affects nearly 1 million people in the U.S. and an estimated 10 million individuals worldwide. Each year, close to 90,000 new cases of Parkinson's disease are diagnosed in the U.S.

In a new study, Jeffrey Kordower, director of the ASU-Banner Neurodegenerative Disease Research Center, and his colleagues unveil pivotal insights into the progression of Parkinson's disease, presenting new hope for patients battling the severely debilitating disorder.

The research highlights the role of a critical protein called tau in the early stages of the disease. The results suggest that aggregates of the tau protein may jump-start processes of neuronal damage and death characteristics of the disease.

The findings challenge the conventional view of Parkinson's disease pathology, which typically focuses on the protein alpha-synuclein as the classic diagnostic hallmark of the disease. The new study illustrates how tau pathology could be actively involved in the degeneration of dopamine-producing neurons in the brain , independent of alpha-synuclein. This revelation could shift the focus of Parkinson's disease research, diagnosis, and treatment.

"Currently, a protein called alpha-synuclein is believed to be the main player in Parkinson's disease pathogenesis," says Kordower, who is also a professor with ASU's School of Life Sciences. "This study highlights that misfolded tau may be the first player in causing the cardinal motor symptoms in the disease."

The paper is published in the journal Brain .

Shattering progression

The progression of Parkinson's disease involves distinct stages, and the timeline can vary significantly among individuals. The typical stages of Parkinson's, as outlined by the Parkinson's Foundation, can help patients understand the changes as they occur.

The disease impacts people in different ways, and not everyone will experience all the symptoms or experience them in the same order or intensity. Some may experience the changes over 20 years or more; for others, the disease advances rapidly.

The progression of the disease is influenced by a combination of genetic and environmental factors. Following a diagnosis, many individuals experience a good response to medications such as levodopa, and this optimal time frame can last for many years. Over time, however, modifications to medication are often needed, and symptoms may intensify.

The prevalence of Parkinson's has doubled in the past 25 years, which may be related to population growth, aging, genetic predisposition, lifestyle changes, and environmental pollution.

A fresh perspective

The tau protein accumulates in two regions: the substantia nigra and putamen, both part of the basal ganglia in the brain. The substantia nigra is responsible for the production of dopamine, which is critical for modulating movement, cognitive executive functions, and emotional limbic activity.

The putamen, a component of the dorsal striatum, is involved in movement initiation, selection, and decision-making, as well as learning, memory, language, and emotion. Dysfunction in the putamen can contribute to various disorders, particularly those related to motor function .

A wide range of physical and mental symptoms characterize Parkinson's disease. These include rhythmic tremors, often beginning in a limb, such as a hand or fingers; slowness of movement, which can lead to difficulty in performing simple tasks; muscle stiffness or rigidity; and difficulties with balance.

In addition to these physical symptoms, Parkinson's disease can also cause various mental and emotional changes, including depression and anxiety, sleep disorders, memory difficulties, fatigue, and emotional changes.

Brain traces of disease

The scientists conducted the study using postmortem brain tissue from older adults who had experienced different degrees of motor impairment. The research analyzed brain tissues from individuals with no motor deficits, mild motor deficits with and without Lewy pathology in the nigral region of the brain, and from individuals clinically diagnosed with Parkinson's disease.

Lewy bodies are abnormal aggregates of the protein alpha-synuclein that accumulate in the brain, and they are a hallmark of several neurodegenerative disorders, including Parkinson's and dementia with Lewy bodies.

In the case of Parkinson's, Lewy bodies are primarily found in the substantia nigra , a region of the brain that is crucial for movement control, which leads to characteristic motor symptoms such as rigidity, tremors and bradykinesia (slow movement).

The study focused on a cohort of subjects with mild motor impairments—not pronounced enough to diagnose Parkinson's, but still significant. Dividing these subjects based on the presence or absence of α-synuclein, researchers found that tau pathology was a common denominator.

The researchers observed that the brain tissue associated with minimal motor deficit demonstrated similar accumulations of tau to those with advanced Parkinson's, suggesting that tau's role occurs early in the disease's evolution. These findings open doors to earlier diagnosis and intervention, potentially slowing or altering the disease's progression.

The research also sheds light on parkinsonism, a condition that mimics Parkinson's disease symptoms but is distinct in its underlying mechanisms. The study suggests that tau pathology in the nigrostriatal region of the brain is a shared characteristic, offering a new lens through which to view and treat various forms of Parkinsonism.

The findings also underscore the potential of targeting tau pathology as a therapeutic approach to Parkinson's disease. Because tau aggregation correlates with motor deficits and degeneration of dopamine-producing regions of the brain, interventions aimed at reducing tau accumulation could offer new hope for altering the disease's trajectory.

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Parkinson's Disease

What is parkinson's disease.

Parkinson's disease (PD) is movement disorder of the nervous system that gets worse over time. As nerve cells (neurons) in parts of the brain weaken, are damaged, or die, people may begin to notice problems with movement, tremor, stiffness in the limbs or the trunk of the body, or impaired balance. As symptoms progress, people may have difficulty walking, talking, or completing other simple tasks. Not everyone with one or more of these symptoms has PD, as the symptoms appear in other diseases as well.

There is no cure for PD, but research is ongoing and medications or surgery can often provide substantial improvement with motor symptoms.

The four primary symptoms of PD are:

• Tremor—Tremor (shaking) often begins in a hand, although sometimes a foot or the jaw is affected first. The tremor associated with PD has a characteristic rhythmic back-and-forth motion that may involve the thumb and forefinger and appear as a “pill rolling.” It is most obvious when the hand is at rest or when a person is under stress. This tremor usually disappears during sleep or improves with a purposeful, intended movement.
• Rigidity—Rigidity (muscle stiffness), or a resistance to movement, affects most people with PD. The muscles remain constantly tense and contracted so that the person aches or feels stiff. The rigidity becomes obvious when another person tries to move the individual's arm, which will move only in short, jerky movements known as “cogwheel” rigidity.
• Bradykinesia—This is a slowing down of spontaneous and automatic movement that can be particularly frustrating because it may make simple tasks difficult. Activities once performed quickly and easily—such as washing or dressing—may take much longer. There is often a decrease in facial expressions (also known as "masked face").
• Postural instability—Impaired balance and changes in posture can increase the risk of falls.

PD does not affect everyone the same way. The rate of progression and the particular symptoms differ among individuals.  PD symptoms typically begin on one side of the body. However, the disease eventually affects both sides, although symptoms are often less severe on one side than on the other.

People with PD often develop a so-called parkinsonian gait that includes a tendency to lean forward, taking small quick steps as if hurrying (called festination), and reduced swinging in one or both arms. They may have trouble initiating movement (start hesitation), and they may stop suddenly as they walk (freezing).

Other problems may accompany PD, such as:

• Depression—Some people lose their motivation and become dependent on family members.
• Emotional changes—Some people with PD become fearful and insecure, while others may become irritable or uncharacteristically pessimistic.
• Difficulty with swallowing and chewing—Problems with swallowing and chewing may occur in later stages of the disease. Food and saliva may collect in the mouth and back of the throat, which can result in choking or drooling. Getting adequate nutrition may be difficult.
• Speech changes—About half of all individuals with PD have speech difficulties that may be characterized as speaking too softly or in a monotone. Some may hesitate before speaking, slur, or speak too fast.
• Urinary problems or constipation—Bladder and bowel problems can occur due to the improper functioning of the autonomic nervous system, which is responsible for regulating smooth muscle activity.
• Skin problems—The skin on the face may become oily, particularly on the forehead and at the sides of the nose. The scalp may become oily too, resulting in dandruff. In other cases, the skin can become very dry. 
• Sleep problems—Common sleep problems in PD include difficulty staying asleep at night, restless sleep, nightmares and emotional dreams, and drowsiness or sudden sleep onset during the day. Another common problem is “REM behavior disorder,” in which people act out their dreams, potentially resulting in injury to themselves or their bed partners. The medications used to treat PD may contribute to some sleep issues. Many of these problems respond to specific therapies.
• Dementia or other cognitive problems—Some people with PD develop memory problems and slow thinking. Cognitive problems become more severe in the late stages of PD, and some people are diagnosed with Parkinson's disease dementia (PDD). Memory, social judgment, language, reasoning, or other mental skills may be affected.
• Orthostatic hypotension—Orthostatic hypotension is a sudden drop in blood pressure when a person stands up from a lying down or seated position. This may cause dizziness, lightheadedness, and, in extreme cases, loss of balance or fainting. Studies have suggested that, in PD, this problem results from a loss of nerve endings in the sympathetic nervous system, which controls heart rate, blood pressure, and other automatic functions in the body. The medications used to treat PD may also contribute.
• Muscle cramps and dystonia—The rigidity and lack of normal movement associated with PD often causes muscle cramps, especially in the legs and toes. PD can also be associated with dystonia—sustained muscle contractions that cause forced or twisted positions. Dystonia in PD is often caused by fluctuations in the body's level of dopamine (a chemical in the brain that helps nerve cells communicate and is involved with movement).
• Pain—Muscles and joints may ache because of the rigidity and abnormal postures often associated with the disease.
• Fatigue and loss of energy—Many people with PD often have fatigue, especially late in the day. Fatigue may be associated with depression or sleep disorders, but it may also result from muscle stress or from overdoing activity when the person feels well. Fatigue may also result from akinesia, which is trouble initiating or carrying out movement.
• Sexual dysfunction—Because of its effects on nerve signals from the brain, PD may cause sexual dysfunction. PD-related depression or use of certain medications may also cause decreased sex drive and other problems.
• Hallucinations, delusions, and other psychotic symptoms can be caused by the drugs prescribed for PD.

Diseases and conditions that resemble PD

PD is the most common form of parkinsonism, which describes disorders of other causes that produce features and symptoms that closely resemble Parkinson's disease. Many disorders can cause symptoms similar to those of PD, including:

• Multiple system atrophy (MSA) refers to a set of slowly progressive disorders that affect the central and autonomic nervous systems. The protein alpha-synuclein forms harmful filament-like aggregates in the supporting cells in the brain called oligodendroglia. MSA may have symptoms that resemble PD. It may also take a form that primarily produces poor coordination and slurred speech, or it may involve a combination of these symptoms. MSA with parkinsonian symptoms is sometimes referred to as MSA-P (or striatonigral degeneration).
• Lewy body dementia is associated with the same abnormal protein deposits (Lewy bodies) found in Parkinson's disease but appears in areas throughout the brain. Symptoms may range from primary parkinsonian symptoms such as bradykinesia, rigidity, tremor, and shuffling walk, to symptoms similar to those of Alzheimer's disease (memory loss, poor judgment, and confusion). These symptoms may fluctuate (vary) dramatically. Other symptoms may include visual hallucinations, psychiatric disturbances such as delusions and depression, and problems with cognition.
• Progressive supranuclear palsy (PSP) is a rare, progressive brain disorder caused by a gradual deterioration of cells in the brain stem. Symptoms may include problems with control of gait and balance (people often tend to fall early in the course of PSP), an inability to move the eyes, and alterations of mood and behavior, including depression and apathy as well as mild dementia. PSP is characterized by clumps of a protein called tau. 
• Corticobasal degeneration (CBD) results from atrophy of multiple areas of the brain, including the cerebral cortex and the basal ganglia. Initial symptoms may first appear on one side of the body, but eventually affect both sides. Symptoms include rigidity, impaired balance, and problems with coordination. Other symptoms may include dystonia that affects one side of the body, cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing). CBD also is characterized by deposits of the tau protein.

Several diseases, including MSA, CBD, and PSP, are sometimes referred to as “Parkinson's-plus” diseases because they have the symptoms of PD plus additional features.

In very rare cases, parkinsonian symptoms may appear in people before the age of 20. This condition is called juvenile parkinsonism. It often begins with dystonia and bradykinesia, and the symptoms often improve with levodopa medication.

Who is more likely to get Parkinson's disease ?

Risk factors for PD include:

• Age—The average age of onset is about 70 years, and the incidence rises significantly with older age. However, a small percent of people with PD have “early-onset” disease that begins before the age of 50.
• Biological sex—PD affects more men than women.
• Heredity—People with one or more close relatives who have PD have an increased risk of developing the disease themselves. An estimated 15 to 25 percent of people with PD have a known relative with the disease. Some cases of the disease can be traced to specific genetic mutations.
• Exposure to pesticides—Studies show an increased risk of PD in people who live in rural areas with increased pesticide use.

The precise cause of PD is unknown, although some cases are hereditary and can be traced to specific genetic mutations. Most cases are sporadic—that is, the disease does not typically run in families. It is thought that PD likely results from a combination of genetics and exposure to one or more unknown environmental factors that trigger the disease.

Parkinson's disease occurs when nerve cells, or neurons, in the brain die or become impaired. Although many brain areas are affected, the most common symptoms result from the loss of neurons in an area near the base of the brain called the substantia nigra. The neurons in this area produce dopamine. Dopamine is the chemical messenger responsible for transmitting signals between the substantia nigra and the next “relay station” of the brain, the corpus striatum, to produce smooth, purposeful movement. Loss of dopamine results impaired movement.

Studies have shown that most people with Parkinson's have lost 60 to 80 percent or more of the dopamine-producing cells in the substantia nigra by the time symptoms appear. People with PD also lose the nerve endings that produce the neurotransmitter norepinephrine—the main chemical messenger to the part of the nervous system that controls many automatic functions of the body, such as pulse and blood pressure. The loss of norepinephrine might explain several of the non-motor features seen in PD, including fatigue and abnormalities of blood pressure regulation.

The protein alpha-synuclein—The affected brain cells of people with PD contain Lewy bodies—deposits of the protein alpha-synuclein. Researchers do not yet know why Lewy bodies form or what role they play in the disease. Some research suggests that the cell's protein disposal system may fail in people with PD, causing proteins to build up to harmful levels and trigger cell death. Additional studies have found evidence that clumps of protein that develop inside brain cells of people with PD may contribute to the death of neurons.

Genetics—Several genetic mutations are associated with PD, including the alpha-synuclein gene, and many more genes have been tentatively linked to the disorder. The same genes and proteins that are altered in inherited cases may also be altered in sporadic cases by environmental toxins or other factors.

Environment—Exposure to certain toxins has caused parkinsonian symptoms in rare circumstances (such as exposure to MPTP, an illicit drug, or in miners exposed to the metal manganese). Other still-unidentified environmental factors may also cause PD in genetically susceptible individuals.

Mitochondria—Mitochondria are the energy-producing components of the cell and abnormalities in the mitochondria are major sources of free radicals—molecules that damage membranes, proteins, DNA, and other parts of the cell. This damage is often referred to as oxidative stress. Oxidative stress-related changes, including free radical damage to DNA, proteins, and fats, have been detected in the brains of individuals with PD. Some mutations that affect mitochondrial function have been identified as causes of PD.

Genes linked to PD

Several genes have been definitively linked to PD:

• SNCA—This gene, which makes the protein alpha-synuclein, was the first gene identified to be associated with Parkinson's. Research findings by the National Institutes of Health (NIH) and other institutions prompted studies of the role of alpha-synuclein in PD, which led to the discovery that Lewy bodies seen in all cases of PD contain clumps of alpha-synuclein. This discovery revealed the link between hereditary and sporadic forms of the disease.
• LRRK2—Mutations in LRRK2 were originally identified in several English and Basque families as a cause of a late-onset PD. Subsequent studies have identified mutations of this gene in other families with PD (such as European Ashkenazi Jewish families) as well as in a small percentage of people with apparently sporadic PD. LRRK2 mutations are a major cause of PD in North Africa and the Middle East.
• DJ-1—This gene helps regulate gene activity and protect cells from oxidative stress and can cause rare, early forms of PD.
• PRKN (Parkin)—The parkin gene is translated into a protein that helps cells break down and recycle proteins.
• PINK1—PINK1 codes for a protein active in mitochondria. Mutations in this gene appear to increase susceptibility to cellular stress. PINK1 has been linked to early forms of PD.
• GBA (glucocerebrosidase-beta)—Mutations in GBA cause Gaucher disease (in which fatty acids, oils, waxes, and steroids accumulate in the brain), but different changes in this gene are associated with an increased risk for Parkinson's disease as well.

How is Parkinson's disease diagnosed and treated?

Diagnosing PD

There are currently no specific tests that diagnose PD. The diagnosis is based on:

• Medical history and a neurological examination
• Blood and laboratory tests to rule out other disorders that may be causing the symptoms
• Brain scans to rule out other disorders. However, computed tomography (CT) and magnetic resonance imaging (MRI) brain scans of people with PD usually appear "normal" or "unremarkable"

In rare cases, where people have a clearly inherited form of PD, researchers can test for known gene mutations as a way of determining an individual's risk of developing the disease. However, this genetic testing can have far-reaching implications and people should carefully consider whether they want to know the results of such tests.

Treating PD

Currently, there is no cure for PD, but medications or surgery can often provide improvement in the motor symptoms.

Drug Therapy

Medications for PD fall into three categories:

• Drugs that increase the level of dopamine in the brain. The most common drugs for PD are dopamine precursors—substances like levodopa that cross the blood-brain barrier and are then changed into dopamine. Other drugs mimic dopamine or prevent or slow its breakdown.
• Drugs that affect other neurotransmitters in the body to ease some of the symptoms of the disease. For example, anticholinergic drugs interfere with production or uptake of the neurotransmitter acetylcholine. These can be effective in reducing tremors.
• Medications that help control the non-motor symptoms of the disease, or the symptoms that don't affect movement. For example, people with PD-related depression may be prescribed antidepressants.

Symptoms may significantly improve at first with medication but can reappear over time as PD worsens and drugs become less effective.

Medications

Levodopa-Carbidopa—The cornerstone of PD therapy is the drug levodopa (also known as L-dopa). Nerve cells can use levodopa to make dopamine and replenish the brain's reduced supply. People cannot simply take dopamine pills because dopamine does not easily pass through the blood-brain barrier, which is a protective lining of cells inside blood vessels that regulate the transport of oxygen, glucose, and other substances in the brain. People are given levodopa combined with another substance called carbidopa. When added to levodopa, carbidopa prevents the conversion of levodopa into dopamine except for in the brain; this stops or diminishes the side effects due to dopamine in the bloodstream. Levodopa-carbidopa is often very successful at reducing or eliminating the tremors and other motor symptoms of PD during the early stages of the disease. People may need to increase their dose of levidopa gradually for maximum benefit. Levodopa can reduce the symptoms of PD but it does not replace lost nerve cells or stop its progression. Initial side effects of levodopa-carbidopa may include:

• Low blood pressure
• Restlessness
• Drowsiness or sudden sleep 

Side effects of long-term or extended use of levodopa may include:

• Hallucinations and psychosis
• Dyskinesia, or involuntary movements such as mild to severe twisting and writhing

Later in the course of the disease, people with PD may begin to notice more pronounced symptoms before their first dose of medication in the morning and between doses as the period of effectiveness after each dose begins to shorten, called the wearing-off effect. People experience sudden, unpredictable “off periods,” where the medications do not seem to be working. One approach to alleviating this is to take levodopa more often and in smaller amounts. People with PD should never stop taking levodopa without their physician's input, because rapidly withdrawing the drug can have potentially serious side effects. 

Dopamine agonists—These mimic the role of dopamine in the brain and can be given alone or with levodopa. They are somewhat less effective than levodopa in treating PD symptoms but work for longer periods of time. Many of the potential side effects are similar to those associated with the use of levodopa, including drowsiness, sudden sleep onset, hallucinations, confusion, dyskinesias, edema (swelling due to excess fluid in body tissues), nightmares, and vomiting. In rare cases, they can cause an uncontrollable desire to gamble, hypersexuality, or compulsive shopping. Dopamine agonist drugs include apomorphine, pramipexole, ropinirole, and rotigotine.  MAO-B inhibitors—These drugs block or reduce the activity of the enzyme monoamine oxidase B, or MAO-B, which breaks down dopamine in the brain. MAO-B inhibitors cause dopamine to accumulate in surviving nerve cells and reduce the symptoms of PD. These medications include selegiline and rasagiline. Studies supported by the NINDS have shown that selegiline (also called deprenyl) can delay the need for levodopa therapy by up to a year or more. When selegiline is given with levodopa, it appears to enhance and prolong the response to levodopa and thus may reduce wearing-off. Selegiline is usually well-tolerated, although side effects may include nausea, orthostatic hypotension, or insomnia. The drug rasagiline is used in treating the motor symptoms of PD with or without levodopa.

COMT inhibitors—COMT stands for catechol-O-methyltransferase and is another enzyme that breaks down dopamine. The drugs entacapone, opicapone, and tolcapone prolong the effects of levodopa by preventing the breakdown of dopamine. COMT inhibitors can decrease the duration of “off periods” of one's dose of levodopa. Side effects may include diarrhea, nausea, sleep disturbances, dizziness, urine discoloration, abdominal pain, low blood pressure, or hallucinations. In a few rare cases, tolcapone has caused severe liver disease, and people taking tolcapone need regular monitoring of their liver function.

Amantadine—This antiviral drug can help reduce symptoms of PD and levodopa-induced dyskinesia. It can be prescribed alone in the early stages of the disease and can be used with an anticholinergic drug or levodopa. After several months, amantadine's effectiveness wears off in up to half of the people taking it. Amantadine's side effects may include insomnia, mottled skin, edema, agitation, or hallucinations. Researchers are not certain how amantadine works in PD, but it may increase the effects of dopamine.

Anticholinergics—These drugs, which include trihexyphenidyl, benztropine, and ethopropazine, decrease the activity of the neurotransmitter acetylcholine and can be particularly effective for tremor associated with PD. Side effects may include dry mouth, constipation, urinary retention, hallucinations, memory loss, blurred vision, and confusion.

When recommending a course of treatment, a doctor will assess how much the symptoms disrupt the person's life and then tailor therapy to the person's particular condition. Since no two people will react the same way to a given drug, it may take time and patience to get the dose right. Even then, symptoms may not be completely alleviated.

Medications to treat motor symptoms of PD

Before the discovery of levodopa, surgery was an option for treating PD. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again considered for people with PD for whom drug therapy is no longer sufficient.

Pallidotomy and Thalamotomy

The earliest types of surgery for PD involved selectively destroying specific parts of the brain that contribute to PD symptoms. Surgical techniques have been refined and can be very effective for the motor symptoms of PD. The most common lesion surgery is called pallidotomy. In this procedure, a surgeon selectively destroys a portion of the brain called the globus pallidus. Pallidotomy can improve symptoms of tremor, rigidity, and bradykinesia, possibly by interrupting the connections between the globus pallidus and the striatum or thalamus. Some studies have also found that pallidotomy can improve gait and balance and reduce the amount of levodopa people require, thus reducing drug-induced dyskinesias.

Another procedure, called thalamotomy, involves surgically destroying part of the thalamus; this approach is useful primarily to reduce tremor.

Because these procedures cause permanent destruction of small amounts of brain tissue, they have largely been replaced by deep brain stimulation for treatment of PD. However, a method using focused ultrasound from outside the head is being tested because it creates lesions without the need for surgery.

Deep Brain Stimulation

Deep brain stimulation (DBS) uses an electrode surgically implanted into part of the brain, typically the subthalamic nucleus or the globus pallidus. Similar to a cardiac pacemaker, a pulse generator (battery pack) that is implanted in the chest area under the collarbone sends finely controlled electrical signals to the electrode(s) via a wire placed under the skin. When turned on using an external wand, the pulse generator and electrodes painlessly stimulate the brain in a way that helps to block signals that cause many of the motor symptoms of PD. (The signal can be turned off using the wand.) Individuals must return to the medical center frequently for several months after DBS surgery in order to have the stimulation adjusted very carefully to give the best results. DBS is approved by the U.S. Food and Drug Administration (FDA) and is widely used as a treatment for PD.

• DBS is primarily used to stimulate one of three brain regions: the subthalamic nucleus, the globus pallidus interna, or the thalamus. Stimulation of either the globus pallidus or the subthalamic nucleus can reduce tremor, bradykinesia, and rigidity. Stimulation of the thalamus is useful primarily for reducing tremor.
• DBS does not stop PD from progressing, and some problems may gradually return. While the motor function benefits of DBS can be substantial, it usually does not help with speech problems, “freezing,” posture, balance, anxiety, depression, or dementia.
• DBS is generally appropriate for people with levodopa-responsive PD who have developed dyskinesias or other disabling “off” symptoms despite drug therapy. DBS has not been demonstrated to be of benefit for “atypical” parkinsonian syndromes such as multiple system atrophy, progressive supranuclear palsy, or post-traumatic parkinsonism, which also do not improve with Parkinson's medications.

Complementary and Supportive Therapies

A wide variety of complementary and supportive therapies may be used for PD, including:

A healthy diet—At this time there are no specific vitamins, minerals, or other nutrients that have any proven therapeutic value in PD. The National Institute of Neurological Disorders and Stroke ( NINDS ) and other components of the NIH are funding research to determine if caffeine, antioxidants, and other dietary factors may be beneficial for preventing or treating PD. A healthy diet can promote overall well-being for people with PD just as it would for anyone else. Eating a fiber-rich diet and drinking plenty of fluids also can help alleviate constipation. A high protein diet, however, may limit levodopa's absorption.

Exercise—Exercise can help people with PD improve their mobility, flexibility, and body strength. It also can improve well-being, balance, minimize gait problems, and strengthen certain muscles so that people can speak and swallow better. General physical activity, such as walking, gardening, swimming, calisthenics, and using exercise machines, can have other benefits. People with PD should always check with their doctors before beginning a new exercise program.

Alternative approaches that are used by some individuals with PD include:

• A NINDS-funded clinical trial demonstrated the benefit of tai chi exercise compared to resistance or stretching exercises in people with PD
• Massage therapy to reduce muscle tension
• Yoga to increase stretching and flexibility
• Hypnosis acupuncture
• The Alexander Technique to optimize posture and muscle activity

Coping with PD

While PD usually progresses slowly, eventually daily routines may be affected—from socializing with friends to earning a living and taking care of a home. These changes can be difficult to accept. Support groups can help people cope with the disease's emotional impact. These groups can provide valuable information, advice, and experience to help people with PD, their families, and their caregivers deal with a wide range of issues, including locating doctors familiar with the disease and coping with physical limitations. A list of national organizations that can help people locate support groups in their communities appears at the end of this information. Individual or family counseling may also help people find ways to cope with PD.

People with PD may also benefit from being proactive and finding out as much as possible about the disease in order to alleviate fear of the unknown and to take a proactive role in maintaining their health. Many people with PD continue to work either full- or part-time, although they may need to adjust their schedule and working environment to accommodate their symptoms.

The average life expectancy of a person with PD is generally the same as for people who do not have the disease. Fortunately, there are many treatment options available for people with PD. However, in the late stages, PD may no longer respond to medications and can become associated with serious complications such as choking, pneumonia, and falls.

Because PD is a slow, progressive disorder, it is not possible to predict what course the disease will take for an individual person.

What are the latest updates on Parkinson's disease ?

The mission of the National Institute of Neurological Disorders and Stroke ( NINDS ) is to seek fundamental knowledge about the brain and nervous system and to use the knowledge to reduce the burden of neurological disease. NINDS, a component of the National Institutes of Health ( NIH ), conducts and supports research on Parkinson's disease are to better understand and diagnose PD, develop new treatments, and ultimately, prevent PD. NINDS also supports training for the next generation of PD researchers and clinicians and serves as an important source of information for people with PD and their families.

Establishing PD research priorities

The NINDS-organized Parkinson's Disease 2014: Advancing Research, Improving Lives  conference brought together researchers, clinicians, patients, caregivers, and nonprofit organizations to develop 31 prioritized recommendations for research on PD. These recommendations are being implemented through investigator-initiated grants and several  NINDS  programs. NINDS and the  NIH 's National Institute of Environmental Health Sciences held the  Parkinson's Disease: Understanding the Environment and Gene Connection  workshop to identify priorities for advancing research on environmental contributors to PD.

Research recommendations for Lewy Body Dementia, including Parkinson's disease dementia, were updated during the NIH Alzheimer's Disease-Related Dementias Summit 2019 (pdf, 2180 KB) .

Key programs and resources

• The Parkinson's Disease Biomarkers Programs (PDBP) , a major  NINDS  initiative, is aimed at discovering ways to identify individuals at risk for developing PD and Lewy Body Dementia and to track the progression of the diseases. It funds research and collects human biological samples and clinical data to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) that will speed the development of novel therapeutics for PD. Goals are improving clinical trials and earlier diagnosis and treatment. Projects are actively recruiting volunteers at sites across the U.S. NINDS also collaborates with the Michael J. Fox Foundation for Parkinson's Research (MJFF) on BioFIND, a project collecting biological samples and clinical data from healthy volunteers and those with PD. 
• The NINDS Morris K. Udall Centers of Excellence for Parkinson's Disease Research program supports research centers across the country that work collaboratively to study PD disease mechanisms, the genetic contributions to PD, and potential therapeutic targets and treatment strategies.
• The Accelerating Medicines Partnership ®  for Parkinson's Disease (AMP ®  -PD) program is a partnership between the NIH, multiple biopharmaceutical and life sciences communities, and nonprofit advocacy organizations to identify and validate biomarkers that can track the progression of PD. It allows scientists to perform large-scale genetic analyses and share data to more quickly bring new medicines to people either with or at risk of PD. 
• The NINDS Intramural Research Program conducts clinical studies to better understand PD mechanisms and develop novel and improve treatments.
• The NINDS Biospecimens Repositories store and distribute DNA, cells, blood samples, cerebrospinal fluid, and autopsy tissue to PD researchers around the world.

Disease research

NINDS  research looks at all aspects of the mechanisms of PD, identifying clues to PD development and its processes, and improving current therapies and testing new ones. Research efforts include:

Cellular Processes—Mutations in alpha-synuclein and dozens of genes (some of which were discovered at  NIH ) are known to either cause PD or modify a person's risk of developing it. Researchers are investigating how the cellular processes controlled by these genes contribute to neurodegeneration, including the toxic accumulation of alpha-synuclein and how the loss of dopamine impairs communication between nerve cells.

Deep Brain Stimulation (DBS)—NINDS  has been a pioneer in the study and development of DBS, which is now considered a standard treatment response to PD medications. Current NINDS-funded projects include research to fine-tune the optimal site within the brain to implant the DBS electrode, studies to better understand the therapeutic effect of DBS on neural circuitry and brain regions affected by PD, and different forms of brain stimulation on different areas of the brain.

Environmental studies—Risk factors such as repeated occupational exposure to certain pesticides and chemical solvents may influence who develops PD. A NINDS-funded research consortium is hunting for environmental risk factors that increase susceptibility to developing PD.

Genetic studies—A better understanding of genetic risk factors is playing a critical role in revealing PD disease mechanisms. A  NINDS  workshop contributed to the development of NeuroX, the first DNA chip that can identify genetic changes in persons at risk for a number of late-onset neurodegenerative diseases, including PD. Another NINDS collaborative, the Consortium On Risk for Early-onset Parkinson's Disease (CORE PD), is trying to identify the genetic factors that contribute to the development of early-onset PD. Current clinical studies include the genetic connection to memory and motor behavior, the search for genes that may increase the risk of PD and related neurodegenerative disorders, and identifying biomarkers for PD.

Motor complications— NINDS  scientists have studied the safety and effectiveness of drugs and interventions in alleviating motor symptoms in people with PD. For example, basic research using adenosine found it could improve motor complications associated with PD. A current NINDS clinical study of motor complications is testing an at-home device to evaluate PD movement symptoms while performing different tasks.

Exercise—Exercise routines are often recommended to help individuals with PD maintain movement and balance necessary for everyday living. Research continues on the role of exercise in slowing the decline of motor function and modifying the course of PD.

Neuroprotective Drugs— NINDS  supports basic, clinical, and translational research aimed at protecting nerve cells from the damage caused by PD. The NINDS-funded NeuroNext Network is designed to test new therapies and to validate biomarkers in a number of neurological disorders, including Parkinson's disease. 

How can I or a loved one help improve care for people with Parkinson's disease ?

Consider participating in a clinical trial so clinicians and scientists can learn more about PD and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed— those who are healthy or may have an illness or disease— of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

For information about participating in clinical research visit NIH Clinical Research Trials and You . Learn about clinical trials currently looking for people with PD at Clinicaltrials.gov .

Where can I find more information about Parkinson's disease ? Information may be available from the following organizations and resources: American Parkinson Disease Association Phone: 718-981-8001 or 800-223-2732 Bachmann-Strauss Dystonia & Parkinson Foundation Phone: 212-509-0995 Davis Phinney Foundation Phone: 303-733-3340 or 866-358-0285 Lewy Body Dementia Association Phone: 404-935-6444 Michael J. Fox Foundation for Parkinson's Research Phone: 800-708-7644 Parkinson Alliance Phone: 609-688-0870 or 800-579-8440 Parkinson's Foundation Phone: 800-473-4636 Parkinson's Resource Organization Phone: 760-773-5628 or 877-775-4111 The Parkinson's Institute and Clinical Center Phone: 408-734-2800 or 800-655-2273

Learn about related topics

• Corticobasal Degeneration
• Lewy Body Dementia
• Multiple System Atrophy
• Progressive Supranuclear Palsy (PSP)

Press Release

Digital transformation, web platform and app aim to improve quality of life for people with parkinson’s disease.

Research News / May 02, 2024

Parkinson’s disease is one of the most prevalent neurodegenerative conditions worldwide. It causes motor impairments such as tremors, slow movement, muscle stiffness, and balance problems. Memory can also worsen as the disease progresses. The individual course of the disease cannot be predicted, so experts recommend regular, close patient monitoring to allow for rapid responses to any changes in symptoms. New technological tools aim to facilitate communication between doctors, caregivers, and patients and improve the care situation. In the ParkProReakt project, researchers from the Fraunhofer Institute for Applied Information Technology FIT are working with partners to create a digital platform and app that, used with wearables, will track the course of the disease in an effort to improve quality of life for Parkinson’s patients.

There are currently about 400,000 people living with Parkinson’s disease in Germany alone. Medications can help with symptoms, but there is no cure. Certain cells responsible for carrying out movements gradually die off, so people with the disease become increasingly limited in their movements and have hand and feet tremors at rest. Getting to the doctor’s office is a challenge for many patients, and there can be long distances involved, especially in rural areas. As a result, patients might only be seen every six months or even less often. New symptoms often go unrecognized by patients and their loved ones, so the information is not passed along to the treatment team. In the ParkProReakt flagship project, researchers from the Fraunhofer Institute for Applied Information Technology FIT and partners (Philipps-Universität Marburg, Justus Liebig University Giessen, Praxis für Neurologie und Psychiatrie Hamburg Walddörfer, AWO Stadtkreis Giessen e. V. and AWO des Landesverband Hamburg e. V., Techniker Krankenkasse, Technische Hochschule Mittelhessen, University of Cologne, Universität zu Lübeck, LiKe Research GmbH, and Portabiles Healthcare Technologies GmbH) plan to foster ongoing communication between doctors and patients and enable regular checkups. The project partners are investigating whether a digital solution can help improve quality of life for patients with Parkinson’s disease. The neurology team at Philipps-Universität Marburg is coordinating the project, which is slated to run until the end of 2025.

Demand-driven care model with a holistic approach

By developing a web platform and a mobile smartphone app that pairs with an Apple Watch via Bluetooth, the partners plan to establish a proactive, demand-driven, cross-sector care model that follows a holistic approach involving healthcare workers and specialists, who can communicate with each other on the platform. The ultimate goal is to ensure better patient care and ease some of the burden on family caregivers, as using the digital solution will help them assess changes in the course of the disease. “The app, which is named Active PD, is used by patients themselves after an initial familiarization phase. The data collected using the app are transmitted to the web platform, which is available to doctors,” explains Daniel Wolferts, a scientist at Fraunhofer FIT. Wolferts and his team are responsible for the human-centric design of both systems, among other aspects. They are working to design the user interface to be user-friendly. “How do we design an app for Parkinson’s patients, and what kind of information do these people want to get? How do we visualize the data in both applications in a user-friendly way for all the different groups concerned, and how do we meet the requirements most effectively? How can we make it so patients can undergo the necessary testing and examinations right on their phone without facing too big a motor challenge? Those are the kinds of questions we’re working on.”

Clinical study with 170 participants

The concept is being validated in clinical studies with 170 patients over a period of six months. One intervention group is to receive the digital solution, while a control group will receive conventional treatment without any added technological tools. The patients are asked to perform standardized Parkinson’s-related tests twice a week using the app and the Apple Watch, which captures their movements via sensors. The tests look mainly at their motor skills and overall condition, helping doctors and other providers to better gauge disease-related symptoms and quickly take appropriate action in response. For example, participants are asked to do finger exercises in front of the smartphone camera, tapping their index finger and thumb together as fast as they can several times in a row. An image recognition feature detects the thumb and forefinger and measures the distance between them during the test. Another exercise involves opening and closing a fist several times at a rapid pace. “Parkinson’s patients have a hard time making these movements quickly and fluidly due to the disease,” the researcher explains. In addition, sensors are used to check whether participants are able to hold their hand still for a certain period without trembling — a challenge for people with Parkinson’s disease. The tests are accompanied by questions about patient wellbeing so support can also be provided at the emotional level as needed. Three color codes — green, yellow, and red — are used to alert the treating physician if a patient’s condition worsens dramatically. The app, which is currently in the prototype stage, can also be used to report incidents such as falls. “We hope our digital solution will give providers a better window on patients’ day-to-day lives and have a positive impact on their quality of life. If we’re successful, we might also ultimately be able to expand the concept to cover other neurological diseases,” Wolferts says.

• Fraunhofer Institute for Applied Information Technology FIT  (fit.fraunhofer.de)
• Further information
• Research News May 2024 - Web platform and app aim to improve quality of life for people with Parkinson’s disease [ PDF  0.32 MB ]

A Skin Test Could Detect Parkinson’s and Related Diseases

New research indicates that a skin biopsy could possibly lead to accurate diagnosis of Parkinson’s and other neurodegenerative diseases.

Currently, there is no single test to diagnose Parkinson’s disease (PD). Doctors rely on symptoms , which can mean a delay in diagnosis as early symptoms can be hard to distinguish from other common ailments. A new study in the Journal of the American Medical Association ( JAMA ) shows that a skin biopsy test can reliably detect Parkinson’s and other related diseases.

Parkinson’s, along with dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF) are four diseases characterized by progressive neurodegeneration and disability. Together this group of diseases are called synucleinopathies because the nerve cells accumulate an abnormal version of the protein alpha-synuclein, which is also referred to as phosphorylated alpha-synuclein (P-SYN).

Previous research indicated that P-SYN could also be found in nerve cells present in the skin. The new JAMA study shows that small amounts of skin taken from the leg, thigh and back of the neck can be analyzed to detect P-SYN in people who have synucleinopathies.

A similar study published last year detected alpha-synuclein in a slightly different test referred to as a seed amplification assay (SAA) analysis . In that study, investigators collected spinal fluid from people with early Parkinson’s. A skin biopsy is considerably less invasive than a lumbar puncture (also known as a spinal tap), which is why this study has generated a lot of interest.

About the Study & Results

The study enrolled 428 participants; 277 were diagnosed with Parkinson’s or another synucleinopathy (DLB, MSA or PAF), along with 151 people who had no history of neurodegenerative disease. Each participant had three skin biopsies that were analyzed in the laboratory.

Of those confirmed to have a synucleinopathy, the biopsies tested positive for P-SYN 92.7% of the time with Parkinson’s, 98.2% with MSA, 96% with DLB, and 100% with PAF. For people who did not have a diagnosis, only 3.3% of the biopsies tested positive for P-SYN.

The researchers also found a correlation between the amount of P-SYN in the biopsies and the severity of the participants’ symptoms.

Biopsy detection of P-SYN was the lowest among those with Parkinson’s (at the rate of 92.7% positive), potentially because there are different subtypes of Parkinson’s or because some genetic causes of Parkinson’s , there may be less P-SYN accumulation. However, study results did not address genetic variations associated with the diagnosis of PD.

However, it’s possible that skin biopsies could detect many cases of Parkinson’s before hallmark symptoms appear — such as tremor and trouble walking . Researchers suspect that P-SYN begins to accumulate in the nerve cells before there are noticeable changes to a person's movement. More research will be needed to confirm this suspicion.

The authors of the study speculated that the 3.3% of the biopsies that tested positive for P-SYN among those who did not have a neurodegenerative disease diagnosis, may indicate the potential for a future synucleinopathy diagnosis. However, longer-term follow-up is needed for confirmation.

More research is needed to determine when P-SYN can be detected in the progression of these diseases, and in those who don’t have symptoms, whether P-SYN detection is always predictive of future disease.

• The study looked for a skin biopsy marker of Parkinson’s and other related neurodegenerative diseases, called phosphorylated alpha-synuclein (P-SYN).
• Among those confirmed to have Parkinson’s, 92.7% of the skin biopsies tested positive for P-SYN.
• Among those who did not have a neurodegenerative diagnosis, only 3.3% of the skin biopsies were positive for P-SYN.
• The amount of P-SYN in the biopsies correlated with the severity of the participants’ symptoms.

What does this mean?

This skin test method could be used to detect Parkinson’s and related diseases before symptoms appear . By identifying the disease before symptoms manifest there is a possibility of developing treatments before the condition progresses. With a reliable way to identify these diseases at their earliest stages, researchers could more effectively evaluate potential treatments and hopefully bring them to people living with PD sooner.

Additionally, because the researchers found a correlation between the amount of P-SYN in the biopsies and the severity of symptoms, the test might be used to test whether potential treatments are working. For example, if a drug treatment reduces P-SYN, it could indicate that the treatment is having an effect.

More research is needed before a skin biopsy would be considered useful for someone who does not have symptoms, as we don’t yet know how early the test could detect whether they will likely have Parkinson’s or other related diseases. We also do not know if some people could have P-SYN in their skin, but never develop symptoms.

What do these findings mean to the people with PD right now?

The skin biopsy test is commercially available  today. It is called the Syn-One Test® and doctors may use it to confirm a synucleinopathy, which may lead to a Parkinson’s diagnosis. A doctor assesses test results alongside other in-office tests and present symptoms to confirm a Parkinson’s diagnosis. If you are already diagnosed with Parkinson’s disease and respond to levodopa treatment, the skin biopsy will likely not add anything to your current management and would not be necessary.

According to the Syn-One Test® manufacturer , Medicare typically covers 80% of the total fee. Insurance may cover all or some of the test fee.

When diagnosing possible Parkinsonism, instead of the Syn-One Test, a doctor may order a DaT scan. Similarly, a DaT scan does not differentiate between the various forms of parkinsonism. Usually if a doctor orders a test to help confirm a Parkinson’s diagnosis, the test is either the skin biopsy test or a DaT scan — not both.

Talk to your Parkinson’s doctor about the Syn-One Test®. If you have already been diagnosed with Parkinson’s and you are responding to therapy, your doctor will most likely not recommend the test. If you are in the process of being diagnosed or confirming a diagnosis, a neurologist or a neurologist with specialty training in movement disorders if available in your region, may consider this test to confirm a diagnosis of a synucleinopathy. Remember that this test is relatively new, so not all Parkinson’s doctors are utilizing it.

The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. Learn more about PD and the topics in this article through our below resources, or by calling our free Helpline at 1-800-4PD-INFO (1-800-473-4636) for answers to your Parkinson’s questions.

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Parkinson's Disease: New theory on the disease's origins and spread

The nose or the gut? For the past two decades, the scientific community has debated the wellspring of the toxic proteins at the source of Parkinson's disease. In 2003, a German pathologist, Heiko Braak, MD, first proposed that the disease begins outside the brain. More recently, Per Borghammer, MD, with Aarhus University Hospital in Denmark, and his colleagues argue that the disease is the result of processes that start in either the brain's smell center (brain-first) or the body's intestinal tract (body-first).

A new hypothesis paper appearing in the Journal of Parkinson's Disease on World Parkinson's Day unites the brain- and body-first models with some of the likely causes of the disease-environmental toxicants that are either inhaled or ingested. The authors of the new study, who include Borghammer, argue that inhalation of certain pesticides, common dry cleaning chemicals, and air pollution predispose to a brain-first model of the disease. Other ingested toxicants, such as tainted food and contaminated drinking water, lead to body-first model of the disease.

"In both the brain-first and body-first scenarios the pathology arises in structures in the body closely connected to the outside world," said Ray Dorsey, MD, a professor of Neurology at the University of Rochester Medical Center and co-author of the piece. "Here we propose that Parkinson's is a systemic disease and that its initial roots likely begin in the nose and in the gut and are tied to environmental factors increasingly recognized as major contributors, if not causes, of the disease. This further reinforces the idea that Parkinson's, the world's fastest growing brain disease, may be fueled by toxicants and is therefore largely preventable."

Different pathways to the brain, different forms of disease

A misfolded protein called alpha-synuclein has been in scientists' sights for the last 25 years as one of the driving forces behind Parkinson's. Over time, the protein accumulates in the brain in clumps, called Lewy bodies, and causes progressive dysfunction and death of many types of nerve cells, including those in the dopamine-producing regions of the brain that control motor function. When first proposed, Braak thought that an unidentified pathogen, such as a virus, may be responsible for the disease.

The new piece argues that toxins encountered in the environment, specifically the dry cleaning and degreasing chemicals trichloroethylene (TCE) and perchloroethylene (PCE), the weed killer paraquat, and air pollution, could be common causes for the formation of toxic alpha-synuclein. TCE and PCE contaminates thousands of former industrial, commercial, and military sites, most notably the Marine Corps base Camp Lejeune, and paraquat is one of the most widely used herbicides in the US, despite being banned for safety concerns in more than 30 countries, including the European Union and China. Air pollution was at toxic levels in nineteenth century London when James Parkinson, whose 269th birthday is celebrated today, first described the condition.

The nose and the gut are lined with a soft permeable tissue, and both have well established connections to the brain. In the brain-first model, the chemicals are inhaled and may enter the brain via the nerve responsible for smell. From the brain's smell center, alpha-synuclein spreads to other parts of the brain principally on one side, including regions with concentrations of dopamine-producing neurons. The death of these cells is a hallmark of Parkinson's disease. The disease may cause asymmetric tremor and slowness in movement and, a slower rate of progression after diagnosis, and only much later, significant cognitive impairment or dementia.

When ingested, the chemicals pass through the lining of the gastrointestinal tract. Initial alpha-synuclein pathology may begin in the gut's own nervous system from where it can spread to both sides of the brain and spinal cord. This body-first pathway is often associated with Lewy body dementia, a disease in the same family as Parkinson's, which is characterized by early constipation and sleep disturbance, followed by more symmetric slowing in movements and earlier dementia, as the disease spreads through both brain hemispheres.

New models to understand and study brain diseases

"These environmental toxicants are widespread and not everyone has Parkinson's disease," said Dorsey. "The timing, dose, and duration of exposure and interactions with genetic and other environmental factors are probably key to determining who ultimately develops Parkinson's. In most instances, these exposures likely occurred years or decades before symptoms develop."

Pointing to a growing body of research linking environmental exposure to Parkinson's disease, the authors believe the new models may enable the scientific community to connect specific exposures to specific forms of the disease. This effort will be aided by increasing public awareness of the adverse health effects of many chemicals in our environment. The authors conclude that their hypothesis "may explain many of the mysteries of Parkinson's disease and open the door toward the ultimate goal-prevention."

In addition to Parkinson's, these models of environmental exposure may advance understanding of how toxicants contribute to other brain disorders, including autism in children, ALS in adults, and Alzheimer's in seniors. Dorsey and his colleagues at the University of Rochester have organized a symposium on the Brain and the Environment in Washington, DC, on May 20 that will examine the role toxicants in our food, water, and air are playing in all these brain diseases.

Additional authors of the hypothesis paper include Briana De Miranda, PhD, with the University of Alabama at Birmingham, and Jacob Horsager, MD, PhD, with Aarhus University Hospital in Denmark.

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Story Source:

Materials provided by University of Rochester Medical Center . Original written by Mark Michaud. Note: Content may be edited for style and length.

Journal Reference :

• E. Ray Dorsey, Briana R. De Miranda, Jacob Horsager, Per Borghammer. The Body, the Brain, the Environment, and Parkinson’s Disease . Journal of Parkinson's Disease , 2024; 1 DOI: 10.3233/JPD-240019

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She had Parkinson's and didn't want to live. Then she got this surgery.

Pam Peters couldn't take it anymore. She couldn't bring a fork to her mouth to feed herself. Couldn't tie her shoes. Write her name. Put pillows in her pillowcases.

"I didn't want to live with the symptoms I was having," the 64-year-old says, grieving her life before. "It just seemed impossible."

The Port Huron, Michigan, resident was initially diagnosed with essential tremor – a nervous system condition that leads to rhythmic and involuntary shaking, according to the Mayo Clinic. But she ultimately found out she actually had Parkinson's disease in February 2022 at another health system, six years after her symptoms began.

Parkinson's is a progressive neurodegenerative disease that worsens over time and is incurable. Patients lose dopamine-producing brain cells important for normal movement. Symptoms include everything from speech changes to impaired balance and stiff muscles, though severity varies by person. It's the second-most common neurological disease behind Alzheimer's .

"I saw myself declining, and it really wasn't a happy time," Peters says. "I was rather close to not wanting to be here. But that has all changed since my surgery."

Peters underwent deep brain stimulation – a procedure where a doctor implants electrodes into a person's brain. It's advisable for some Parkinson's patients who have an uncontrolled resting tremor respond unpredictably to medication. The electrodes help regulate movement – a game-changer for patients like Peters and others amid the ongoing fight for medical breakthroughs for neurologic conditions.

Parkinson’s arrived in her 20s. Now, she's thankful for a procedure she was once scared of.

"(Parkinson's is) something that people live with every single day," says Dr. Adam Kuhlman, the medical director of Corewell Health’s Movement Disorders Program in Southeast Michigan. "They don't go very long without being reminded that those symptoms are right there, that are impacting their ability to execute daily activities."

'We've been able to provide her relief'

Parkinson's is typically treated with levadopa , a dopamine-producing medication. Kuhlman otherwise encourages patients to exercise, get enough sleep and seek out social support. But when medication doesn't result in the desired effects – i.e. in Peters' case – other options enter the conversation. Hence deep brain stimulation, which was first approved about 25 years ago for multiple conditions, including Parkinson's.

Peters had a few, rough painful days after the surgery in November, but saw results right away after Kuhlman activated the electrodes a month post-op.

"We've been able to give her and provide her the relief of her symptoms that we would otherwise have been getting with oral medications, but at least for the time being, she's not requiring any oral medications that were causing her so much difficulty," Kuhlman says.

More neurologic conditions: Bruce Willis and my dad received the same aphasia diagnosis. Then everything changed.

Patients will typically follow up frequently within the first six months, then they stretch out to every few months to every six months from there.

As for the future of Parkinson's treatment: "A much more attainable goal is having something that's going to be disease -modifying, that is something that's going to be able to slow down progression. Thus far, we don't have anything that's currently available."

Of course, "sometimes it's discouraging not having something more to offer," he says. "But part of the reason why I got into the field to begin with was that this is something where we're seeing so much more attention, we're seeing so much more funding and so much more research and we're just primed for a breakthrough."

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'I don't want to lose what I have'

Now, Peters is more back to her old self. She ate rice on a fork the other night. She's working out three to four times a week and wants to train for the Senior Olympics in her town.

"It's really been incredibly gratifying for me as her physician to see the turnaround that we've had, and finding the right treatment for her and seeing her go from really seeming to struggle and be kind of down with the whole process, to functioning much closer to the way that she was hoping she was going to and being able to participate in the things that she wanted to participate, especially in terms of being physically active," Kuhlman says.

But most important: Between participating in Parkinson's group therapy and the deep brain stimulation treatment, Peters has hope.

"I can't get every moment in enough," she says. "I can't hug enough babies . I want it all right now. I don't want to lose what I have either."

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May 2, 2024 | Mike Enright '88 (CLAS), University Communications

UConn Students Earn NSF Graduate Research Fellowships

The program supports outstanding students in NSF-supported disciplines who are pursuing research-based master’s and doctoral degrees

Cynthia Webster (left) and Charlotte Chen (right), seen here posing for a photo in front of Wilbur Cross on April 24, 2024, are among the UConn students who earned a National Science Foundation Graduate Research Fellowship (NSF-GRFP) grant this year. (Sydney Herdle/UConn Photo)

A total of 10 students with ties to the University of Connecticut have recently earned National Science Foundation Graduate Research Fellowships (NSF-GRFP). Those 10 include three undergraduates, three graduate students (including two who earned their undergraduate degrees at UConn) and four UConn alumni.

The oldest graduate fellowship of its kind, the NSF-GRFP recognizes and supports outstanding students in NSF-supported disciplines who are pursuing research-based master’s and doctoral degrees at accredited institutions in the United States. In addition to a three-year annual stipend of $37,000, plus another $12,000 paid to the student’s home institution, fellows have access to a wide range of professional development opportunities over the course of their graduate careers.

The Graduate Research Fellowships are highly competitive, with annual acceptance rates of about 16% from among more than 12,000 applicants.

“The application for the NSF-GRFP is extremely demanding. To succeed, students must be able to articulate themselves not only as researchers, but as future leaders in their academic disciplines,” says Vin Moscardelli, director of UConn’s Office of National Scholarships and Fellowships. “This year’s results once again reveal the combination of talent, ambition, and support that exists here at UConn.”

UConn’s 10 recipients lead all New England public universities for 2024. UConn has produced at least ten NSF-GRFP recipients in eight of the past nine years. The school also had nine students, five graduate and four alumni, who earned honorable mention laurels in this cycle.

“The NSF Graduate Research Fellowship is truly a great achievement,” says Pamir Alpay, UConn’s vice president for research, innovation and entrepreneurship. “It acknowledges our students’ talent and their potential to shape the future of science and technology. More than that, UConn’s GRFP recipients reflect our commitment to excellence and offering outstanding research opportunities to our students. Our students are competitive for the GRFP because of the sustained hard work our exceptional faculty have put into building our research programs and sharing their expertise with our students.”

The three UConn graduate student recipients are:

Lorraine Pérez-Beauchamp ‘23 (CLAS) earned her undergraduate degree from UConn in biological sciences. She is a first-year graduate student in ecology and evolutionary biology, and her faculty mentor is associate professor Sarah Knutie. Pérez-Beauchamp is currently performing research in the Galápagos Islands.

Cynthia Webster ’20 (CLAS) is in her second year as graduate student in ecology and evolutionary biology, working under the direction of associate professor Jill Wegrzyn. Her research interests reside at the intersection of computational biology, genome evolution, and conservation genetics. In her fellowship, she will build the first pangenome for the butternut, which is endangered due to its low tolerance to a non-native fungal pathogen.

“In graduate school, it’s common to experience imposter syndrome and question whether you’re making a significant contribution to society,” says Webster. “So many talented individuals apply for the GRFP each year, but only a handful are awarded. As a young scientist, this recognition is incredibly validating.”

Bre-Anna Willis is a first-year graduate student in chemistry studying chemical synthesis. Her faculty mentor is associate professor of chemistry Gaël Ung. Willis earned her undergraduate degree in 2023 from the University of Tennessee at Chattanooga.

The three UConn undergraduate recipients are:

Charlotte Chen ’24 (ENG & CLAS) is a senior from Weston, pursuing dual degrees in materials science & engineering and molecular & cell biology.  Her research in the lab of associate professor of chemical and biomolecular engineering Kelly Burke aims to modify silk films with antibacterial monomers to potentially prevent catheter-associated urinary tract infections.

“Being awarded an NSF-GRFP means that I get a lot more freedom with my doctoral studies– what my research project is, who my research advisors are, and where I want to conduct the research,” says Chen.

She will be a doctoral student at Brown in the fall to pursue a degree in biomedical engineering with the long-term goal of a career in the biotech industry.

Sila Inanoglu ’24 (CLAS) is an ecology major and her faculty mentor is also Knutie. She is a member of Knutie’s lab this year and is working on the group’s Nest Parasite Community Science project. Her research investigates the direct and indirect effects of alpha-pinene, the volatile compound in pine needles, on ectoparasite resistance in tree swallows. After graduation, she will be staying a UConn as a doctoral student in Knutie’s lab.

“Winning the NSF-GRFP feels surreal,” says Inanoglu. “I did not even pursue STEM until my sophomore year at UConn and being awarded the NSF-GRFP has made me realize how far I have come. Being in this field as a student and researcher has been some of the most fulfilling and exciting work I have gotten to do. I am beyond excited to be able to continue my research and scientific outreach goals with NSF’s support.”

Paxton Tomko ’24 (CLAS) is a molecular and cell biology major and her faculty mentor is Assistant Professor of Molecular and Cell Biology/Microbiology Geo Santiago-Martínez. In the fall, she will be starting a master’s in oceanography at UConn Avery Point, working with Professor of Marine Sciences Pieter Visscher. Tomko’s research interests are in geobiology and astrobiology and is interested in stromatolites as biosignatures and the role that methanogens play in microbial mats.

The four UConn alumni who earned NSF Graduate Research Fellowships are Brigid Bernier ’23 (CLAS) , who is now a graduate student at the University of Oklahoma; Samuel Degnan-Morgenstern ’22 (ENG) , who is now a graduate student at the Massachusetts Institute of Technology; Jackson Kaszas ’23 (ENG) , who is now a graduate student at Rutgers University; and Rebecca Lee ’22 (ENG) , who is now a graduate student at the University of Texas.

The  Office of National Scholarships & Fellowships  (ONSF) is a resource for students interested in learning more about the NSF Graduate Research Fellowship and other prestigious scholarships and fellowships that support graduate study in all fields. ONSF is part of Enrichment Programs and is open to all graduate and undergraduate students at the University, including students at the regional campuses. For more information contact Vin Moscardelli, Director of UConn’s  Office of National Scholarships and Fellowships .

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