Potential Parkinson’s Therapy ABBV-0805 Enters Phase 1 Testing in Healthy Volunteers

 MARCH 15, 2019 BY ALICE MELÃO 

AbbVie has launched a Phase 1 trial in the United States to assess the safety and tolerability of an investigational antibody targeting alpha-synuclein called ABBV-0805 in healthy volunteers.

This study comes after the U.S. Food and Drug Administration approved an investigational new drug application for ABBV-0805 in February.

Findings of this initial Phase 1 trial will provide critical information for the design and progression of future clinical studies on this antibody as a potential disease-modifying treatment for patients with Parkinson’s disease.

Formerly known as BAN0805, ABBV-0805 was initially engineered and developed by BioArctic. It is a monoclonal antibody designed to specifically bind and destroy toxic aggregates of alpha-synuclein protein, which are known to contribute to the developmentof Parkinson’s disease.

In preclinical studies, this investigational antibody effectively decreased the levels of alpha-synuclein clumps by 65% compared with placebo. In addition, treatment with ABBV-0805 also delayed disease progression, reduced Parkinson’s-associated motor symptoms, and improved overall survival in a mouse model of Parkinson’s disease.

BioArctic and AbbVie established a strategic collaboration agreement in 2016 for the further development and future marketing rights on BioArctic’s portfolio of antibodies directed against alpha-synuclein.

More recently, in December 2018, AbbVie exercised its option to acquire full rights over ABBV-0805. The company is now responsible for the clinical program and regulatory approval of the new antibody as a treatment for Parkinson’s and other potential indications.

“It is gratifying that our partner AbbVie has started the first clinical trial, a Phase 1 study, with ABBV-0805,” Gunilla Osswald, PhD, CEO of BioArctic, said in a press release. “We are now looking forward to ABBV-0805 moving forward in the clinical program and developing into a therapy with the potential to provide meaningful advances for patients with Parkinson’s disease.”

BioArctic will continue to develop other potential therapies targeting misfolded and abnormal proteins linked to Parkinson’s disease in the continued collaboration with AbbVie.

“I am looking forward to continuing the successful partnership with the ambition to deliver a new innovative disease modifying treatment to improve the quality of life for the large number of patients with Parkinson’s disease,” Osswald said in a previous press release.

https://parkinsonsnewstoday.com/2019/03/15/abbv-0805-enters-phase-1-trial/

Nature Walks and Gardening Improve Overall Health

MARCH 15, 2019 Dr. CBY DR. C IN COLUMNS

Nature,” the “N” of the CHRONDI Creed, has always been a part of my life. One doctor told me, “Your strong history of exercise and nature has kept Parkinson’s at bay.”

I was an avid hiker, cyclist, and rock collector in my youth. As I headed into my gray-haired years with Parkinson’s disease (PD), I moved from these activities to building and maintaining gardens around my home. I have always felt healthier when gardening, without knowing about the research that supports my experience. I have since discovered many studies that show nature walks and gardening contribute to improvements in overall health.

Dr. C at work in his garden. (Courtesy of Dr. C)

Humans have interacted with and depended on nature for millennia. We have only migrated toward becoming city dwellers in relatively recent history. Returning to our roots (pun intended) can bestow many health benefits on us. Living next to “green environments” has been shown to have both mental and physical health advantages. Walks in parks, particularly when mindfulness is used — known as “forest bathing” — can have positive effects on well-being.

I can attest to the benefits of this practice, both personally and as a teacher of mindfulness. Some people have trouble meditating while sitting, and a mindful walk in the woods can help to quiet their minds and bodies. Connecting with nature has holistic effects, and it doesn’t have to take hours out of a busy life — just five minutes can make a difference.

Humans have always built sacred sites on or near places of exceptional natural beauty. Our ancestors harnessed the awe that we experience when viewing a magnificent mountain or a beautiful ocean scene to open a doorway into the soul. But these doorways are obscured by hordes on the highways, multitudes straining the subway, and the super speed of technology stripping away our humanity. It is so easy to get lost in our modern culture and forget an intrinsic part of being human: the “nature” in human nature. Setting aside time each week to walk mindfully in a green environment is the first step to reconnecting with ourselves.

Gardening occupies more time than a stroll in the park does, but there are additional physical benefits to be found with getting your hands dirty. It’s an excellent activity for people with PD when the routine is adapted for safety and severity of symptoms.

I consider myself a “landscape painter,” and gardening is my main form of exercise. Building garden beds and pathways are my way of constructing a personal green space. I have a relationship with the plants in my garden. This connection is so important to me that when I moved house, I took hundreds of my plants with me.

Caring for my garden and enjoying the beauty of blooms and foliage is an enriching experience. I feel awe and a sense of falling in love with its beauty. Gardening has overall health benefits that help me to manage the symptoms of my chronic disease. It’s never too late to benefit from exercise, and if you’re planning to be more active, gardening can be a fun way to get moving again.

How do you connect with nature to improve your health while living with a chronic disease?

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Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

https://parkinsonsnewstoday.com/2019/03/15/nature-walks-gardening-health/

Leukemia Treatment Tasigna Improves Brain Dopamine Use In Parkinson’s Patients, Trial Finds

MARCH 15, 2019   BY JOSE MARQUES LOPES, PHD 

Treatment with a single dose of the leukemia therapy Tasigna (nilotinib) improves the brain’s ability to use dopamine in people with Parkinson’s by reducing inflammation and levels of toxic alpha-synuclein, according to Phase 2 trial results.

The research, “Pharmacokinetics and pharmacodynamics of a single dose Nilotinib in individuals with Parkinson’s disease,” was published in the journal Pharmacology Research & Perspectives.

Previous studies by the team at Georgetown University Medical Center showed that a low dose of Novartis’ Tasigna is able to reach the brain, ease inflammation and degrade misfolded alpha-synuclein — the main component of Parkinson’s characteristic Lewy bodies — in animal models of neurodegenerative disease. Tasigna also increased levels of dopamine — the neurotransmitter found at reduced levels in this disease — and improved motor and cognitive function.

A pilot study in 12 individuals with Parkinson’s disease dementia and dementia with Lewy bodies suggested that this therapy could effectively treat Parkinson’s motor and non-motor symptoms, while also increasing dopamine metabolism — its use in the brain — and lowering alpha‐synuclein levels.

The scientists now studied the pharmacological profile of Tasigna in patients with Parkinson’s. The study, part of a Phase 2 trial (NCT02954978), included 75 participants, randomized into five groups of 15, who received either placebo or one of four doses of Tasigna — 150 mg, 200 mg, 300 mg, or 400 mg.

At one, two, three, and four hours after treatment, researchers measured Tasigna’s levels in the blood and cerebrospinal fluid (CSF, the liquid surrounding the brain and spinal cord). They also measured DOPAC and homovanillic acid (HVA) — both byproducts of dopamine metabolism — oligomers (small bits of alpha-synuclein), and the TREM-2 protein, an indicator of neuroinflammation. Levels of alpha-synuclein oligomers are typically increased and are potentially toxic in Parkinson’s disease.

The findings revealed that the ability of Tasigna to enter the brain was independent of the dose used. However, the optimal dose to increase the levels of DOPAC and HVA compared to placebo, thereby dopamine use, was 200 mg.

“This is exciting because this kind of potential treatment for Parkinson’s could increase use of a patient’s own dopamine instead of using or periodically increasing drugs that mimic dopamine,” Charbel Moussa, PhD, the study’s senior author, said in a press release.

The same 200 mg dose significantly increased the CSF level of TREM-2. The lowest dose (150 mg) induced a significant decrease in plasma levels of alpha-synuclein at two hours of treatment, while the 200 mg and 400 mg doses reduced the ratio of oligomers to total alpha‐synuclein in the CSF.

“This suggests an elevated beneficial immune activity that targets misfolded alpha-synuclein for destruction,” said Moussa, also the scientific and clinical research director of the Translational Neurotherapeutics Program at Georgetown.

“Taken together, 200 mg Nilotinib appears to be an optimal single dose that concurrently reduces inflammation and engages surrogate disease biomarkers, including dopamine metabolism and alpha‐synuclein,” researchers stated.

Overall, the effects of Tasigna in the brain are “unprecedented for any drug now used to treat Parkinson’s,” Moussa said.

The scientists said that the effects seen at lower but not higher doses may be due to Tasigna having multiple targets, which may cause lower specificity if too much of the therapy is used.

Moussa said alpha-synuclein helps release dopamine from the tiny vesicles containing this neurotransmitter. However, in Parkinson’s, the increasing production of misfolded alpha-synuclein impairs dopamine breakdown.

In preclinical studies, Tasigna improved dopamine release by triggering brain cells to attack the misfolded protein, which could help explain the increase in TREM-2 and dopamine breakdown in the CSF of patients, Moussa noted.

Fernando Pagan, MD, the trial’s principal investigator, agreed that Tasigna appears to lessen toxic alpha-synuclein and brain inflammation, while preserving dopamine and dopamine-producing nerve cells.

“Whether or not, or how much, the drug demonstrates improved clinical outcomes will be determined when the [Phase 2] clinical trial results are in,” Pagan said.

https://parkinsonsnewstoday.com/2019/03/15/leukemia-treatment-tasigna-improves-brain-dopamine-use-in-parkinsons-patients-trial-finds/

Synchronizing Finger Taps to Regular Beats Improves Gait of Parkinson’s Patients, Study Suggests

 MARCH 14, 2019 BY JOSE MARQUES LOPES, PHD IN NEWS.

Parkinson’s disease patients improved their gait after undergoing training in which they tapped their fingers in synchrony to regular beats set at a faster pace than their walking speed, a study has found.

The research, “Rhythmic priming across effector systems: A randomized controlled trial with Parkinson’s disease patients,” appeared in the journal Human Movement Science.

Clinical studies have shown that rhythmic auditory stimulation (RAS), using rhythm and music, significantly improved gait and upper extremity function for stroke, Parkinson’s disease, traumatic brain injury, and other conditions.

Auditory stimuli have been used in the motor rehabilitation of patients with Parkinson’s disease, who increased their walking speed, stride length, and stability after RAS training, an approach that uses rhythmic cues to improve motor function.

It is still unclear whether short-term RAS of arm or finger movements also improves gait, although studies have suggested that rhythmic arm movements while walking enable arm-leg coordination to improve gait.

Therefore, researchers at the University of Toronto and Colorado State University decided to investigate whether RAS training of arm or finger movements would modulate gait speed in 37 patients with idiopathic (of unknown cause) Parkinson’s disease.

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A group of 11 patients (with seven men, a mean age of 68.4 years, and disease duration of 4.8 years) underwent a four-minute training — three one-minute blocks separated by 30 seconds — in which arm or finger movements were performed in synchrony to beats (using a metronome) set to a 20% faster pace than their pre-training walking speed. The patients used the index finger of the least affected hand for tapping. Auditory stimuli were delivered with a speaker placed one meter away from the participant.

A separate group of 14 participants (with six men, a mean age of 64.2 years, and disease duration of 7.7 years) was asked to swing both arms in an alternating manner in synchrony with the metronome. Both finger-tapping and arm-swing tasks were performed with participants seated in an armless chair.

The 12 patients in the control group — with four men, a mean age of 67.3 years, and disease duration of 11.7 years — did not receive any training.

All participants were on Parkinson’s medication and had a Hoehn & Yahr (H&Y) scalescore of one or two, which indicates that their balance was not impaired.

Gait assessments pre- and post-training required walking on a 14-meter flat walkway at the participant’s preferred walking speed with no auditory cueing.

The results revealed a significant 9.5% increase in gait velocity after the finger-tapping training, from an average of 69.75 meters/min before training to 76.03 meters/min post-training. No differences were seen in the arm-swing and control groups.

Patients who underwent finger-tapping training also showed an 8% increase in gait cadence, or the number of steps per minute — from 109.25 to 117.5 — unlike those in the other groups. No post-training differences in stride length were seen in any group.

“The present study supports the hypothesis that rhythmic priming is possible across effector systems by demonstrating that (RAS) training of finger movements had immediate effects on gait velocity and cadence of patients with Parkinson’s,” the researchers wrote.

“The present findings have direct implications for motor rehabilitation and extend the current application of rhythmic-based interventions,” they added.

https://parkinsonsnewstoday.com/2019/03/14/synchronizing-finger-taps-regular-beats-improve-gait-parkinsons-study/

Manganese and Parkinson's: Mechanism may explain link

 Ana Sandoiu    March 15, 2019

New research helps explain how and why manganese exposure could lead to Parkinson's.

New research, published in the journal Science Signaling, details the mechanism through which exposure to manganese can trigger protein misfolding in the brain — which may, in turn, lead to Parkinson's-like symptoms. The findings may enable an earlier diagnosis of the neurological condition.

Manganese is an essential nutrient present in "legumes, pineapples, beans, nuts, tea, and grains."

In the human body, manganese aids blood sugar regulation, bone formation, and immunity.

However, exposure to excessive levels of manganese may trigger Parkinson's-like neurological symptoms.

Manganese builds up in the basal ganglia area of the brain.

Researchers have known about these links between manganese and Parkinson's for decades, but new research helps elucidate the mechanisms behind these associations.

Anumantha Kanthasamy, the Linda Lloyd Endowed Chair of Neurotoxicology at Iowa State University in Ames, led the new research. 

Manganese helps transfer a faulty protein

Parkinson's disease is characterized by clumps formed by misfolded alpha-synuclein protein. These protein aggregates are toxic to neurons.

Kanthasamy and colleagues set out to investigate how these misfolding proteins might interact with manganese to trigger the progression of Parkinson's.

To do so, they examined data from mice and blood serum samples collected from eight welders. As a group, welders have a higher risk of prolonged manganese exposure. The research also examined a control group of 10 people.

The analyses revealed that welders with exposure to manganese had higher levels of misfolded alpha-synuclein, which puts them at a higher risk of Parkinson's.

Additional cell culture tests showed that misfolded alpha-synuclein was secreted through small vesicles called exosomes into the extracellular space. In other words, the vesicles enabled the proteins to travel from cell to cell and further spread the misfolded protein.

The scientists also isolated alpha-synuclein-containing exosomes from alpha-synuclein-expressing cells that had exposure to manganese and delivered them to a brain area in the mice called the corpus striatum. This induced Parkinson's-like symptoms in the mice.

Manganese seemed to accelerate the "cell-to-cell transmission" of alpha-synuclein, which, in turn, led to neurotoxicity. Kanthasamy and colleagues explain:

"Together, these results indicate that [manganese] exposure promotes [alpha-synuclein] secretion in exosomal vesicles, which subsequently evokes proinflammatory and neurodegenerative responses in both cell culture and animal models."

"[W]e identified a possible mechanism involving the exosome-mediated, cell-to-cell transmission of [alpha-synuclein] during exposure to the environmental neurotoxicant," write the authors.

Findings may lead to earlier detection

According to the National Institutes of Health (NIH), around 50,000 individuals in the United States receive a diagnosis of Parkinson's each year, and 500,000 people currently live with the condition.

Though the condition does not yet have a cure, diagnosing it earlier may prevent irreversible brain damage and help accelerate human clinical trials of new drugs.

The results that Kanthasamy and colleagues have just published may help scientists devise a new diagnostic test for Parkinson's that could detect the disease much earlier on. The results may also help scientists test how effective new Parkinson's drugs are.

"As the disease advances, it's harder to slow it down with treatments," Kanthasamy says. He adds: "Earlier detection, perhaps by testing for misfolded alpha-synuclein, can lead to better outcomes for patients. Such a test might also indicate whether someone is at risk before the onset of the disease."

However, the study authors also caution that their findings are still experimental, and that such a diagnostic test may not be available for years.

https://www.medicalnewstoday.com/articles/324715.php

Tingle' wearable device improves position tracking accuracy utilizing thermal sensors

March 05. 2019
by The Child Mind Institute

In a new study published in npj Digital Medicine, a team led by Child Mind Institute researchers report that a wearable tracking device they developed achieves higher accuracy in position tracking using thermal sensors in addition to inertial measurement and proximity sensors. The wrist-worn device, called Tingle, was also able to distinguish between behaviors directed toward six different locations on the head. 

The paper, "Thermal Sensors Improve Wrist-worn Position Tracking," provides preliminary evidence of the device's potential use in the diagnosis and management of excoriation disorder (chronic skin-picking), nail-biting, trichotillomania (chronic hair-pulling), and other body-focused repetitive behaviors (BFRBs).

The researchers, led by Arno Klein, Ph.D., Director of Innovative Technologies, Joseph Healey Scholar, and Senior Research Scientist in the Center for the Developing Brain at the Child Mind Institute, collected data from 39 healthy adult volunteers by having them perform a series of repetitive behaviors while wearing the Tingle. The Tingle was designed by the Institute's MATTER Lab to passively collect thermal, proximity and accelerometer data.

Dr. Klein and colleagues found that the thermal sensor data improved the Tingle device's ability to accurately distinguish between a hand's position at different locations on the head, which would be useful in detecting clinically relevant BFRBs. BFRBs are related to a variety of mental and neurological illnesses, including autism, Tourette Syndrome and Parkinson's Disease.

"Body-focused repetitive behaviors can cause significant harm and distress," said Dr. Klein. "Our findings are quite promising because they indicate that the thermal sensors in devices like the Tingle have potential uses for many different types of hand movement training, in navigation of virtual environments, and in monitoring and mitigating repetitive, compulsive behaviors like BFRBs."

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Story Source:

Materials provided by The Child Mind Institute. Note: Content may be edited for style and length.

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Journal Reference:

1. Jake J. Son, Jon C. Clucas, Curt White, Anirudh Krishnakumar, Joshua T. Vogelstein, Michael P. Milham, Arno Klein. Thermal sensors improve wrist-worn position tracking. npj Digital Medicine, 2019; 2 (1) DOI: 10.1038/s41746-019-0092-2

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https://www.sciencedaily.com/releases/2019/03/190314123122.htm

An impaired sense of smell can signal cognitive decline, but 'smell training' could help

March 15,2019   by Anna Wolf And Alex Bahar-Fuchs,  The Conversation

An inhibited sense of smell means we may not taste our food as well. Credit: shutterstock.com

As we age, we often have problems with our ability to smell (called olfactory dysfunction). Older people might not be able to identify an odour or differentiate one odour from another. In some cases they might not be able to detect an odour at all.Odour identification difficulties are common in people with neurodegenerative diseases, including Alzheimer's disease.

In the absence of a known medical cause, an impaired sense of smell can be a predictor of cognitive decline. Older people who have difficulty identifying common odours have been estimated to be twice as likely to develop dementia in five years as those with no significant smell lossOlfactory dysfunction is often present before other cognitive symptoms appear, although this loss can go undetected.

Beyond being a potential early indicator of Alzheimer's disease, olfactory problems can pose safety risks, such as not being able to smell gas, smoke, or rotten food. Smell ability is also strongly linked to our ability to taste, so impairments can lead to decreased appetite and therefore nutritional deficiencies. In turn, olfactory deficits can decrease quality of life and increase the risk of depression.But there is emerging evidence that olfactory or "smell training" can improve ability to smell.

These findings may offer some hope for older adults experiencing olfactory difficulties and an associated decline in quality of life. How is our sense of smell linked to our brainsThe process of smelling activates the complex olfactory network in the brain. When we smell a rose, for example, receptors in the nose detect the many molecules that make up the rose's odour. 

This information is then sent to the many areas of the brain (including the olfactory bulb and olfactory cortex, the hippocampus, the thalamus and the orbitofrontal cortex) that help us process the information about that odour.

To name the rose, we access our stored knowledge of its pattern of odour molecules, based on past experience. So identifying the smell as belonging to a rose is considered a cognitive task.

What is smell training?

Smell training has been studied in various animals, from flies to primates. Animals exposed to multiple odours develop an increased number of, and connections between, brain cells. This process has been shown to enhance learning and memory of odours.

In humans, olfactory training has typically involved smelling a range of robust odours representing major odour categories – flowery (such as rose), fruity (lemon), aromatic (eucalyptus) or resinous (cloves). Participants may be asked to focus their attention on particular odours, try to detect certain odours, or note odour intensities.

Generally, training is repeated daily for several months. Periods over three monthsare suggested for older adults.

This training has been shown to improve people's ability to identify and tell the difference between smells. To a lesser extent, it can help with odour detection in people with various forms of smell loss, including those with a brain-derived impairment such as a head injury or Parkinson's disease.

Importantly, one recent study of olfactory training in older adults found it not only improved performance on identifying smells, but was also associated with improvement in other cognitive abilities.

For example, those who undertook smell training had improved verbal fluency(improved ability to name words associated with a category), compared to control participants who completed Sudoku exercises.

How does smell training work?

Neuroplasticity, our brains' ability to change continuously in response to experience, may be key to how smell training works. 

Neuroplasticity involves the generation of new connections and/or the strengthening of existing connections between neurons (brain cells), which in turn may lead to changes in thinking skills or behaviour. We can see evidence of neuroplasticity when we practise a skill such as playing an instrument or learning a new language.

The olfactory network is considered particularly neuroplastic. Neuroplasticity may therefore underlie the positive results from smell training, both in terms of improving olfactory ability and boosting capacity for other cognitive tasks.

Could smell training be the new brain training?

Brain training aiming to maintain or enhance cognitive function has been extensively studied in older people with dementia or at risk of it. 

Established cognitive training approaches generally train participants to use learning strategies with visual or auditory stimuli. To date, formal cognitive training has not been attempted using smells. 

However, using the considerable neuroplasticity of the olfactory network and evidence-based cognitive training techniques, both olfactory and cognitive deficits may be targeted, particularly in older adults at risk of dementia. It seems possible we could train our brains through our noses.

Provided by The Conversation

https://medicalxpress.com/news/2019-03-impaired-cognitive-decline.html

Researchers explore link between metal exposure and Parkinson’s symptoms

March 13,  2019

Anumantha Kanthasamy

Quote

“As the disease advances, it’s harder to slow it down with treatments. Earlier detection, perhaps by testing for misfolded alpha-synuclein, can lead to better outcomes for patients. Such a test might also indicate whether someone is at risk before the onset of the disease.”

Anumantha Kanthasamy, Clarence Hartley Covault Distinguished Professor in veterinary medicine and the Eugene and Linda Lloyd Endowed Chair of Neurotoxicology

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AMES, Iowa – A new study from Iowa State University biomedical researchers illuminates the biological processes by which exposure to some metals can contribute to the onset of Parkinson’s-like symptoms.

The study, published today in the peer-reviewed journal Science Signaling, focuses on the metal manganese, which has a range of industrial uses as an alloy. Anumantha Kanthasamy, a Clarence Hartley Covault Distinguished Professor in veterinary medicine and the Eugene and Linda Lloyd Endowed Chair of Neurotoxicology, said the research details how manganese exposure can lead to misfolded proteins in the brain, which cause a neurological disease. Kanthasamy said the findings could lead to earlier detection of the disease and better outcomes for patients.

Kanthasamy said small amounts of manganese are necessary for the proper functioning of the human body, but too much exposure has been linked with neurological symptoms much like those experienced by patients with Parkinson’s Disease. Links between manganese and neurological disorders have been noted since the 1950s, Kanthasamy said, because of the tendency of manganese to accumulate in brain tissues.

The latest study found that manganese combines with a protein in the brain called alpha- synuclein. Previous studies showed the protein was susceptible to misfolding, but Kanthasamy and his colleagues set out to discover how it interacted with manganese and how that interaction facilitates the progression of disease. The researchers found the pathological form of misfolded alpha-synuclein proteins get packaged into vesicles, which allow the misfolded proteins to transfer from cell to cell to propagate the protein-seeding activity. These vesicles provoke inflammation of tissues and can lead to a neurodegenerative response, the study found.

The study drew on data gathered from mice as well as blood serum samples from welders provided by clinicians at Penn State University. The study found welders exposed to manganese had increased misfolded alpha-synuclein serum content, meaning the welders are at a higher risk for developing Parkinson’s symptoms, Kanthasamy said.

The research could contribute to a new assay, or medical test, to detect the presence of misfolded alpha-synuclein proteins. This could lead to earlier detection of Parkinson’s Disease and a way to gauge the effectiveness of drugs designed to slow the disease.

“As the disease advances, it’s harder to slow it down with treatments,” Kanthasamy said. “Earlier detection, perhaps by testing for misfolded alpha-synuclein, can lead to better outcomes for patients. Such a test might also indicate whether someone is at risk before the onset of the disease.”

Kanthasamy cautioned the research is still at an experimental stage, meaning it could be years before such an assay could be available.

Dilshan S. Harischandra, a former member of Kanthasamy’s lab who now works at the University of Pennsylvania, was the lead author of the study. Kanthasmy, chair of the Department of Biomedical Sciences in the ISU College of Veterinary Medicine, was the senior author of the study. The study was supported by a grant from the National Institute of Environmental Health Sciences.

https://www.news.iastate.edu/news/2019/03/12/manganeseparkinsons