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I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
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Thursday, May 24, 2018

Early hearing loss could pave the way for dementia,' study says

May 24, 2018 

The majority of us will think nothing of listening to loud music via headphones, or standing in the front row, next to the speakers, at a rock concert. But these habits may lead to subtle hearing loss, which, research now shows, may affect the brain in undesirable ways.

Beware of minor hearing problems early in life; they may lead to cognitive impairment as you grow older.

Every day of our lives, we face being exposed to loud noises — particularly those of us who live in busy cities.
These are not normally loud enough to harm our hearing. But if we are consistently exposed to sounds that break a certain noise threshold, it may, in time, cause some amount of hearing loss.
The unit used to measured sound intensity is decibels, and the Centers for Disease Control and Prevention (CDC) offer examples of which types of sounds are harmless and which may endanger hearing, based on decibel level.
Normal conversation or soft background noises — such as the humming of an air conditioning unit — amount to about 60 decibels. Louder noises that you may find annoying — such as the sound of the washing machine running — amount to 70 decibels. The noise of city traffic could rise to about 80–85 decibels.
Exposure to noises above 85 decibels (but under 120 decibels) over a long period of time can harm the hearing. Such noises could be music listened to at maximum volume using headphones, sitting close to the speakers at a music concert or at the movies, and working with power tools.
The unit used to measured sound intensity is decibels, and the Centers for Disease Control and Prevention (CDC) offer examples of which types of sounds are harmless and which may endanger hearing, based on decibel level.
Normal conversation or soft background noises — such as the humming of an air conditioning unit — amount to about 60 decibels. Louder noises that you may find annoying — such as the sound of the washing machine running — amount to 70 decibels. The noise of city traffic could rise to about 80–85 decibels.
Exposure to noises above 85 decibels (but under 120 decibels) over a long period of time can harm the hearing. Such noises could be music listened to at maximum volume using headphones, sitting close to the speakers at a music concert or at the movies, and working with power tools.

Extremely loud noises over 120 decibels can cause immediate hearing loss.

Recently, researchers from Ohio State University in Columbus have found that young adults with minor hearing loss display changes in brain activity that are normally only seen in old age.
"Hearing loss, even minor deficits, can take a toll in young people — they're using cognitive resources that could be preserved until much later in life," notes lead researcher Yune Lee.
Most concerning, this early hearing loss could pave the way for dementia."
Yune Lee  

The team's findings were recently published in the journal eNeuro.

Brain activity characteristic of aging

Initially, Lee and his colleagues had set out to complete different kind of project. They recruited 35 participants aged between 18 and 41 who agreed to undergo functional MRI scans while listening to sentences of varying complexities.
The researchers were interested in monitoring and comparing brain activity when a listener had to process messages with a simple structure versus more complicated sentences that likely involved a different kind of cognitive effort.
Yet their study took a different turn as they noted something surprising about some of their young adult participants.
Yet after conducting the fMRI scans, they noticed that the participants with subtle hearing problems actually processed the messages they heard differently from their peers. And not just that, but their brain activity in this context was similar to that of aging listeners.
Specifically, healthy young adults with no hearing problems only use the left hemisphere of the brain to process heard information. But the participants with minor hearing impairments actually showed activity in both the left and the right hemispheres of their brains.
In the case of the latter, the right frontal cortex became active — something normally seen only in older people.
"This isn't about the ear — it's about the brain, the cognitive process, and it shouldn't be happening until people are at least older than 50," Lee explains.

Twice as likely to have dementia'

The study authors explain that, normally, healthy young adults only use the left brain hemisphere when engaged in language comprehension tasks. As people age, however, they start to engage the right frontal part of the brain too, as they put more effort into processing spoken language.
"But in our study," says Lee, "young people with mild hearing decline were already experiencing this phenomenon."
"Their brains already know that the perception of sound is not what it used to be and the right side starts compensating for the left," he adds.
It is hard to say how this might impact these individuals later in life, but Lee and team worry that the hearing issues may only worsen, affecting comprehension. And, this can hasten the development of neurodegenerative conditions such as dementia.
"Previous research," says Lee, "shows that people with mild hearing loss are twice as likely to have dementia. And those with moderate to severe hearing loss have three to five times the risk."
"We can't be sure," he continues, "but we suspect that what happens is you put so much effort into listening you drain your cognitive resources, and that has a negative effect on your thinking and memory and that can eventually lead to dementia."
For these reasons, Lee advises young adults to look after their hearing more carefully and avoid exposing themselves to situations that are likely to have undesired consequences.
"Letting [hearing loss] happen early in your life," Lee cautions, "could be like spending your retirement money when you're in your 30s. You're going to need that down the road."

Feds Eye New Rules On Flying With Service Animals

 by Shaun Heasley | May 22, 2018

The U.S. Department of Transportation is soliciting public comment as it considers changes to regulations governing service animals on airplanes. (Josie Lepe/Bay Area News Group/TNS)

Citing “significant concerns” from people with disabilities and others, federal airline regulators are weighing big changes to rules for service animals in flight.
The U.S. Department of Transportation said this month that it wants feedback from the public on possible alterations to service animal regulations under the Air Carrier Access Act.
Specifically, transportation officials want to know if emotional support animals, psychiatric service animals and other types of service animals should be treated differently from each other and if there should be limits on the species, size or number of service animals that can fly with a person. In addition, the Transportation Department notice asks if owners should be required to confirm that their service animal is trained and questions if leashes or harnesses should be mandated.
The request for public comment comes after several major air carriers moved in recent months to issue new policies on service and emotional support animals following a significant uptick in passengers bringing such animals aboard. Delta Air LinesUnited Airlines and American Airlines have all announced policies since the start of the year that they say are designed to curtail problems with biting, urination and other misbehavior.
“The department recognizes the integral role that service animals play in the lives of many individuals with disabilities and wants to ensure seamless access to air transportation for individuals with disabilities while also helping to deter the fraudulent use of animals not qualified as service animals,” the Transportation Department said in announcing its effort to seek public feedback.
Previously, a Transportation Department advisory committee tasked with addressing accessibility was unable to reach a consensus on how to tackle the issues surrounding service animals on airliners.
In addition to soliciting comment, transportation officials also issued an “interim statement of enforcement priorities” this month related to service animals outlining the agency’s current procedures.
The Advance Notice of Proposed Rulemaking on Traveling By Air with Service Animals is up for public comment for 45 days.
To Comment:

What is formication?

 23 May 2018   By Jamie Crawford

Formication is the sensation of having insects crawling on or under the skin. The name comes from the Latin word "formica," which means ant.
Formication is a tactile hallucination, which means a person feels a physical sensation, but there is no physical cause. The sensation can lead to itching, which may be worse at night and can be severe enough to impact on a person's quality of life.
Feeling sensations on the skin with no physical stimulation is a type of paresthesia, which may also include burning, tingling, numbness, and cold.
Formication is linked to several other medical conditions, as well as withdrawal from some drugs and substances.
Causes of formication
Several conditions can cause formication. They include:
It is possible that lower estrogen levels during perimenopause and menopause may also cause formication.
Formication can sometimes occur when a person is going through withdrawal from drugs, especially from opiates. The list below includes some of the drugs that can cause formication during withdrawal.
  • Ritalin
  • Wellbutrin
  • Lunesta
  • opioid pain medications, such as codeine or morphine
  • some antidepressants, such as SSRIs
  • Tramadol
  • cocaine
  • heroin
  • methamphetamine
  • MDMA
Formication linked to drug withdrawal is usually temporary and should resolve when a person recovers from withdrawal.
If the sensation continues or is very intense, it could be due to drug psychosis. This may cause a person to believe that they have an actual infestation of bugs in their skin.
Alcohol withdrawal can also cause formication. People may experience visual hallucinations too, as well as other symptoms. It is, therefore, best to have a doctor or other professional oversee alcohol withdrawal, as symptoms may be severe.


It is essential to give the doctor full and honest answers at the appointment so that they can provide an accurate diagnosis. They may want to know:
  • any other symptoms that are present in addition to formication
  • at what time of day the crawling sensations occur
  • what was happening when the sensations first started
  • any medication being taken
  • whether a person has used any recreational drugs
  • if a person drinks alcohol
A doctor might also want to rule out scabies. Scabies is an infection of tiny mites that burrow in the skin. They cause extreme itching and leave a rash.


Treatment for formication will depend on the underlying cause. A topical cream, such as hydrocortisone, might lessen the itching for some people. Moisturizers or barrier creams may also help by keeping the skin healthy and hydrated.
It could also be worth placing an ice pack on the affected areas, which can provide a soothing effect for immediate relief.
If the cause of the formication is Parkinson's disease, shingles, or fibromyalgia, a doctor will prescribe appropriate medication and may create a long-term treatment plan.
If medication is the cause, a doctor can usually recommend alternatives. Sometimes, an antihistamine, such as Zyrtec or Benadryl, can help reduce the sensations of formication.
Some antihistamines can make people drowsy, so it is important to read the labels and ask a pharmacist questions about the side effects before using them.
If formication is linked to recreational drug use, quitting and finding professional support for withdrawal can resolve symptoms.

Possible complications

If a person is experiencing formication, they may be prone to constant scratching. This can break the skin, which can allow bacteria to enter and possibly cause infections to develop.

Formication can cause poor quality sleep and tiredness.
Potential complications of scratching include:
Other complications of formication include:
  • tiredness
  • frustration
  • poor sleep quality
  • depression
  • anxiety
  • problems concentrating
  • aching or feeling stiff
It is important to seek medical advice for any and all complications. Feeling tired or depressed can make formication worse.


Formication is a symptom of an underlying condition, so fully treating this condition should typically get rid of the symptoms. The condition may be physical, psychological, or related to substance misuse.
If the cause is not apparent, screening out possible conditions could detect something previously undiagnosed.
Speaking openly and honestly with a doctor will allow them to develop a personalized treatment plan to improve the condition as soon as possible.

FoxFeed Blog: President Speaks on High Price of Prescription Drugs

Posted by  Allyse Falce, May 21, 2018

People with Parkinson's disease (PD) are well aware that prompt access to effective medications is vital to managing symptoms and maintaining a high quality of life. But this is possible only if drugs are affordable. On Friday, May 11, the president addressed the nation and introduced "American Patients First," which he billed the first proposal of its kind to tackle the United States' notoriously high drug prices(two to six times higher than the rest of the world).
The president indicated that he plans to work closely with the secretary of Health and Human Services and the commissioner of the Food and Drug Administration to accomplish the items laid out in the proposal. (Earlier this week, the FDA published a list of drug makers that may be delaying the development of generic alternatives to their products). Go to:
As reported by several news outlets, while the president's report outlined several areas for potential activity -- including increasing competition, better negotiation, and creating incentives to lower list prices -- the published proposal does not commit the administration to specific action steps. According to The Wall Street Journal, "The administration generally is still seeking input on many questions it hopes to tackle," adding, "Expect a flurry of activity, proposals and regulations from the administration this year on drug pricing." For now, at least, it is too soon to report on whether specific policy changes may be forthcoming or stand to benefit people with Parkinson's.
(Congress also is involved in attempts to lower drug prices, introducing numerous pieces of legislation intended to increase access to medications. 
The Know the Lowest Price Act of 2018 eliminates barriers preventing pharmacists from telling people when their drugs would be less expensive if they paid in cash rather than using insurance. The Restoring the Patient's Voice Act of 2017 addresses insurance company regulations that require patients to try a less expensive drug before being granted coverage for the original medication they were prescribed. This bill creates an exceptions process to allow patients quicker access to the original drug.)
The Foundation will continue to advocate in Washington to ensure patients have access to the care they need to manage their Parkinson's disease. Stay tuned to our blog for the latest updates on our public policy work and any news about efforts to lower drug prices.

FoxFeed Blog: Policymakers Expand Telemedicine Services for Veterans

 Posted by  Stephanie Katz,   May 24, 2018

It's estimated that more than 80,000 U.S. veterans are living with Parkinson's disease (PD). Research tells us that certain events in the line of service, such as exposure to chemicals or traumatic brain injury, are associated with elevated Parkinson's risk. Today's veterans with PD, and those who may be diagnosed in the future, need access to comprehensive care to help manage their disease.
Earlier this month, the Department of Veterans Affairs (VA) instituted a new ruling to increase access to telemedicine for veterans who receive their care through the VA health system. Telemedicine -- the delivery of health care services and information via electronic methods (two-way video, smartphones, etc.) -- can help people with PD receive the care they need when they have difficulty traveling (due to symptoms like decreased mobility, imbalance or walking issues). And, because doctors familiar with Parkinson's disease may be limited in certain areas, telemedicine helps overcome geographic barriers to care.
The new rule allows VA doctors to provide care across state lines via telemedicine, which was not possible before this change. Therefore, if the closest VA doctor that meets a veteran's care needs is located out of state, telemedicine can be used to conduct virtual visits. Not only do telemedicine services help reduce costs for veterans, and all patients, they also can make Parkinson's care more accessible, efficient and personalized, which could lead to improved quality of life.
The Foundation submitted comments to the VA to push for this new change and conducted several visits with members of Congress to educate them on the importance of telemedicine. We'll continue to work with the Parkinson's community to advocate for policies that promote broad access to these services for all people living with PD.
Want to take action on public policy issues that matter to you? Check out our advocacy page for information on how to contact your lawmakers.
Go to:

Brain Training Decreases Severity of Parkinson’s Freezing of Gait, Study Reports


Brain training reduces the severity and duration of freezing of gait and improves cognition and daytime sleepiness in Parkinson’s patients, a study shows.
Freezing of gait is a symptom of Parkinson’s disease and occurs when patients temporarily feel as if their feet are glued to the floor and hesitate before stepping forward. This often leads to falls and lower quality of life. Studies have shown a connection between freezing of gait and impaired attention and cognitive control.
Researchers in Australia conducted a double-blind trial with Parkinson’s patients who self-reported freezing of gait and had no signs of dementia. Patients were randomly assigned to either cognitive training intervention (20 patients) or an “active control” (18 patients).
Cognitive training consisted of exercises where participants were asked to get up from a chair and walk to a spot marked with a box 5 meters away. Conditions in which patients completed different tasks involving the box were evaluated. Two trials of each condition were completed, one with a left turn and one to the right.
The conditions included: one in which participants walked to the box, turned 180 degrees, and returned to their chair; one where they completed a 540-degree turn in the box before returning to the chair; one in which they shuffled around the box, keeping their inside foot to the outside of the box; and a dual task, where they did the same exercise as the first 180-degree condition, but also completed a cognitive task as they walked, either naming aloud the months backwards or multiples of nine or seven.
Study interventions were conducted twice weekly for seven weeks. Each session took two hours.
The initial 30-45 minutes were common to both groups and included education about a number of topics related to Parkinson’s. Patients undergoing cognitive training then conducted computer tasks targeting processes such as attention, working memory, and brain processing speed. Patients in the active control group completed nonspecific computer tasks.
Investigators primarily evaluated the percentage of time spent frozen during cognitive training, which was analyzed while subjects were both on and off dopaminergic medications. Researchers also assessed several other measures, including mood, well-being, anxiety and depression, sleep quality, and quality of life.
For patients on dopaminergic medication, results showed that those on cognitive training had a significant decrease in the severity of their freezing of gait compared with patients in the active control group. Cognitive training also led to improvements in processing speed and reduced daytime sleepiness.
In contrast, no differences were found when comparing patients not taking regular dopaminergic treatment.
“These results add to the growing body of evidence showing that [cognitive training] is a useful therapeutic technique worthy of continued exploration in [Parkinson’s],” the researchers wrote in the study.
“We believe there is reason to be hopeful for the use of these trials in the future,” Simon Lewis, MD, the study’s senior author and a professor of cognitive neuroscience at the University of Sydney’s Brain and Mind Centre, said in a press release.
He also emphasized the positive feedback from participants and family members, and added that “the results of this pilot study highlight positive trends, and the importance of nonpharmacological trials involving cognitive training has become increasingly clear.”
The researchers also noted the importance of their finding that improvements only occur in patients on dopaminergic medication, “the normal day-day state for patients with Parkinson’s,” said Courtney Walton, PhD, the study’s lead author, who is now at the University of Queensland.
“While more research is needed to better understand and establish these findings, it’s likely that participants in the off- dopaminergic state were too impaired to benefit from any of the potential changes initiated through cognitive training,” Walton said.

Scientists Unraveling How Movement is Translated Into Desired Action


The findings of a Harvard University study are furthering understanding of the mechanisms involved in movement disorders and may open new therapeutic opportunities to treat Parkinson’s disease.
The mouse study, “The Striatum Organizes 3D Behavior via Moment-to-Moment Action Selection,” was published in the journal Cell.
The brain relies on the balanced activity of two nerve cell populations located in a specific region of the brain — the striatum — to achieve accurate control of body movement. The striatum functions as the coordinating center for motor and action planning. In Parkinson’s disease, striatum nerve cells are those most affected, which partly explains the motor symptoms that characterize the disease.
A previous study identified two groups of nerve cells in the striatum that have opposing activities to control key aspects of movement; those are called direct pathway and indirect pathway neurons.
While direct pathway cells select actions and can trigger movement, the activation of indirect pathway cells works as a stop signal, inhibiting unwanted behaviors. However, some studies suggest both pathways are activated at the same time.
“That didn’t make sense based on what we’ve long thought each pathway did,” the study’s lead author Jeffrey Markowitz, said in a press release.
To evaluate the dynamic activity of both cell populations, Harvard Medical School researchers used a technology called MoSeq (short for motion sequencing) developed by study’s senior author Sandeep Robert Datta. This technology films three-dimensional movements of the mice and uses machine learning to analyze the movements into basic patterns lasting only a few hundred milliseconds apiece. The researchers named those ultra-fast movements “syllables.”
Mice were genetically engineered to display different glowing colors in direct and indirect pathway neurons upon activation, allowing researchers to accurately analyze the simultaneous activity of both cell populations as mice performed several actions.
When mice changed their behavior — from running to stopping, for example — the activity of both pathways increased, which is in agreement with data from previous studies. But when they looked at the syllables identified by the MoSeq system, they found the pattern of activity of both pathways was not the same.
Instead, direct or indirect pathway cells dominated some particular syllables. The association between the type of cell that was activated and syllables was so pronounced that the team could effectively identify syllables based on the pathway activity alone.
To further characterize the role of these cells, the team induced brain injuries in the mice, targeting only the striatum. After a week of recovery, they re-analyzed animals’ behavior and compared them with that of healthy animals.
Mice with brain lesions in this specific area also were able to perform normal syllables, such as sniffing, running, rearing, and turning. However, their brains were unable to sequence these movements correctly.
“… behavioral syllables are associated with characteristic and pathway-specific neural dynamics. These dynamics represent key 2D and 3D movement parameters … the striatum plays a key role in choosing which … behavioral syllable to express at any given moment,” researchers wrote.
“This underscores the importance of order in piecing movements together toward a desired outcome,” Datta said. “Even if you’re able to move your body correctly, if you can’t put actions in the correct order, it’s hard to do even the most basic of things.”
The researchers believe that with additional studies and improved technology it will be possible not only  to replicate these results, but expand this reported relationship between syllables and neural activity to other parts of the brain that control movement.
In addition, these findings may help promote the development of new treatments for Parkinson’s disease and other neurodegenerative disorders in which basic movements become extremely difficult as disease progresses.
“We hope that future work emanating from these findings would address more specifically what exactly happens in these cell types when neurodegenerative disorders rob people’s brains of their ability to generate actions and action sequences.” Datta said. “We believe our observations set the stage for both unraveling how movement gets translated into desired action, and propel us forward in our ability to understand and, eventually, treat devastating neurodegenerative disorders where this process goes awry,” he added.

Study suggests brainwave link between disparate disorders

 May 24, 2018 by Stephen Fontenot, University of Texas at Dallas

This summary figure shows the spatial distribution of theta-beta and theta-gamma cross-frequency coupling as they relate to different syndromes. Credit: University of Texas at Dallas

A brainwave abnormality could be a common link between Parkinson's disease, neuropathic pain, tinnitus and depression—a link that authors of a new study suggest could lead to treatment for all four conditions.

Dr. Sven Vanneste, an associate professor in the School of Behavioral and Brain Sciences at The University of Texas at Dallas, is one of three authors of a paper in the journal Nature Communications regarding thalamocortical dysrhythmia (TCD), a theory that ties a disruption of brainwave activity to the symptoms of a wide range of neurological disorders.
Vanneste and his colleagues—Dr. Jae-Jin Song of South Korea's Seoul National University and Dr. Dirk De Ridder of New Zealand's University of Otago—analyzed electroencephalograph (EEG) and functional brain mapping data from more than 500 people to create what Vanneste believes is the largest experimental evaluation of TCD, which was first proposed in a paper published in 1996.
"We fed all the data into the computer model, which picked up the brain signals that TCD says would predict if someone has a particular disorder," Vanneste said. "Not only did the program provide the results TCD predicted, we also added a spatial feature to it. Depending on the disease, different areas of the brain become involved."
Brainwaves are the rapid-fire rhythmic fluctuations of electric voltage between parts of the brain. The defining characteristics of TCD begin with a drop in brainwave frequency—from alpha waves to theta waves when the subject is at rest—in the thalamus, one of two regions of the brain that relays sensory impulses to the cerebral cortex, which then processes those impulses as touch, pain or temperature.
A key property of alpha waves is to induce thalamic lateral inhibition, which means that specific neurons can quiet the activity of adjacent neurons. Slower theta waves lack this muting effect, leaving neighboring cells able to be more active. This activity level creates the characteristic abnormal rhythm of TCD.
"Because you have less input, the area surrounding these neurons becomes a halo of gamma hyperactivity that projects to the cortex, which is what we pick up in the brain mapping," Vanneste said.
While the signature alpha reduction to theta is present in each disorder examined in the study—Parkinson's, pain, tinnitus and depression—the location of the anomaly indicates which disorder is occurring.
"If it's in the auditory cortex, it's going to be tinnitus; if it's in the somatosensory cortex, it will be pain," Vanneste explained. "If it's in the motor cortex, it could be Parkinson's; if it's in deeper layers, it could be depression. In each case, the data show the exact same wavelength variation—that's what these pathologies have in common. You always see the same pattern."
EEG data from 541 subjects was used. About half were healthy control subjects, while the remainder were patients with tinnitus, chronic pain, Parkinson's disease or major depression. The scale and diversity of this study's data set are what set it apart from prior research efforts.
"Over the past 20 years, there have been pain researchers observing a pattern for pain, or tinnitus researchers doing the same for tinnitus," Vanneste said. "But no one combined the different disorders to say, 'What's the difference between these diseases in terms of brainwaves, and what do they have in common?' The strength of our paper is that we have a large enough data sample to show that TCD could be an explanation for several neurological diseases."
With these results in hand, the next step could be a treatment study based on vagus nerve stimulation—a therapy being pioneered by Vanneste and his colleagues at the Texas Biomedical Device Center at UT Dallas. A different follow-up study will examine a new range of psychiatric diseases to see if they could also be tied to TCD.
For now, Vanneste is glad to see this decades-old idea coming into focus.
"More and more people agree that something like thalamocortical dysrhythmia exists," he said. "From here, we hope to stimulate specific  areas involved in these diseases at alpha frequencies to normalize the brainwaves again. We have a rationale that we believe will make this type of therapy work."
More information: Sven Vanneste et al. Thalamocortical dysrhythmia detected by machine learning, Nature Communications (2018). DOI: 10.1038/s41467-018-02820-0 
Journal reference: Nature Communications

Early synaptic dysfunction found in Parkinson's Disease

May 24, 2018 by Will Doss, Northwestern University

LRRK2 patient-derived dopaminergic neurons display synaptic defects. Neurons derived from healthy human controls showed normal synaptic vesicle densities in the synaptic terminal (upper image), whereas LRRK2 patients displayed sparse and enlarged vesicles (asterisks, lower image) indicative of defective synaptic function. Credit: Northwestern University

Northwestern Medicine scientists identified a cellular mechanism that leads to neurodegeneration in patients with Parkinson's disease, according to a study published in Proceedings of the National Academy of Sciences.

Dimitri Krainc, MD, Ph.D., chair and Aaron Montgomery Ward Professor of Neurology, was the senior author of the study, which demonstrated a link between defective synaptic vesicle endocytosis and accumulation of toxic oxidized .
When it accumulates in the brain, oxidized dopamine has been shown to mediate the death of dopamine-containing neurons, causing the common motor symptoms observed in Parkinson's disease (PD) patients, according to previous research conducted by Krainc and published in Science. While people naturally lose  as they age, patients with PD lose a much larger number of these neurons and the remaining cells are no longer able to compensate for the loss of brain function, leading to disease.
"In our prior work, we found that oxidized dopamine is toxic to neurons," said Krainc, who is also director of the Center for Neurogenetics. "In this paper, we further explain how such oxidized dopamine is formed in synaptic terminals of neurons from patients with Parkinson's disease."
The process begins when a protein called auxilin is dysregulated by another protein, a mutated form of LRRK2. Normally, auxilin regulates the process of synaptic vesicle endocytosis, a mechanism that neurons use to replenish the chemical signals needed to communicate with each other.
In the current study, scientists found that mutations in LRRK2 lead to dysfunctional auxilin and consequently impaired synaptic vesicle endocytosis. This manifests in inefficient packaging of dopamine into synaptic vesicles and an eventual buildup of dopamine in Parkinson's neurons.
This pool of "extra" dopamine can be rapidly oxidized and become toxic to dopamine , according to the study.
"These findings suggest that early therapeutic intervention in dysfunctional presynaptic terminals may prevent downstream toxic effects of oxidized dopamine and neurodegeneration in PD," Krainc said.
In addition, these studies of genetic forms of Parkinson's disease help identify converging pathways in the pathogenesis of sporadic and familial PD, highlighting the importance of investigating such cellular mechanisms to identify specific targets for therapy.
"This study is another example of how the emergence of genetic causes of Parkinson's has helped us understand how  develops and where to focus to identify key pathways and targets for drug development," Krainc said.
More information: Maria Nguyen et al. LRRK2 phosphorylation of auxilin mediates synaptic defects in dopaminergic neurons from patients with Parkinson's disease, Proceedings of the National Academy of Sciences(2018). DOI: 10.1073/pnas.1717590115