New AI Model May Improve Use of Touchscreens by Patients with Parkinson’s, Other Disabilities

user interface

Finnish and Japanese researchers have developed a new algorithmic approach to user interface optimization that takes individual differences into account. This approach could be beneficial for patients with Parkinson’s disease or other disabilities.

The research, “Ability-Based Optimization of Touchscreen Interactions,” was published in the journal IEEE Pervasive Computing.

Among the limitations presented by users with disabilities are essential tremors, characterized by involuntary and rhythmic shaking, most often when using the hands for simple tasks, dyslexia, which impairs the ability to read words of the interface, and dementia.

Strategies to overcome these limitations could involve increasing the size of user interface elements and grouping functions together, reducing the amount of text in the screen and making sure it is correct,  creating designs that require as little previous knowledge as possible, and prioritizing frequent tasks.

“The majority of available user interfaces are targeted at average users. This ‘one size fits all’ thinking does not consider individual differences in abilities — the aging and disabled users have a lot of problems with daily technology use, and often these are very specific to their abilities and the circumstances,” Jussi Jokinen, one of the study’s co-authors, said in a press release.

Approaches to improve the user interface require an accurate model of the user, Jokinen observed. “Previously, designers did not have detailed models that are based on psychological research and can be used to predict how different individuals perform in interactive tasks,” he said.

The scientists developed a new model of interaction, which combines psychological research on finger pointing and eye movements to predict limitations in text entry speed, typing, and proofreading.

By simulating a user with essential tremors, the researchers predicted that using the common Qwerty keyboard is almost impossible, because more than half of all typed keys are typos. “We chose to simulate and optimize for essential tremor, because it makes text entry very difficult,” Jokinen said.

“We connected the text entry model to an optimizer, which iterates through thousands of different user interface designs. No real user could of course try out all these designs. For this reason it is important that we could automatize the evaluation with our computational model,” he added.

This resulted in an interface predicted to be superior for individuals with essential tremors; the simulated user did not make any entry errors. The optimized layout was then tested with a person with essential tremors, who was able to type almost error-free messages.

“This is of course just a prototype interface, and not intended for consumer market,” Jokinen said. “I hope that designers pick up from here and with the help of our model and optimizer create individually targeted, polished interfaces.”

“While more empirical work is needed to evaluate the results, the first evidence acquired in this paper is promising,” the researchers wrote. Future work should test the design for dyslexics, they said.

Beyond the confirmed validity of the model in essential tremor and text entry, scientists also may use it for other disabilities and tasks. “For example, we have models for simulating how being a novice or an expert with an interface impacts users’ performance,” Jokinen said.

The effects of memory impairment in learning and everyday use of interfaces also may be addressed, he added.

“The important point is that no matter the ability or disability, there must be a psychologically valid theory behind modeling it. This makes the predictions of the model believable, and the optimization is targeted correctly,” Jokinen said.

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Duopa Can Help Parkinson’s Patients Manage Impulse Control Disorders, Study Shows

Duopa for impulse control

AbbVie’s Duopa can reduce impulse control disorders in patients with advanced Parkinson’s disease and mild-to-moderate neuropsychiatric problems, a study shows.

The research, “Improvement of impulse control disorders associated with levodopa-carbidopa intestinal gel treatment in advanced Parkinson’s disease,” was published in the Journal of Neurology.

Parkinson’s disease is characterized by the death of brain cells that produce the signaling molecule dopamine — a chemical that facilitates communication between nerve cells.

Dopamine replacement agents can reduce movement symptoms of the disease. The treatments can lead to side effects, however. One is impulse control disorders, such as compulsive gambling, buying, sexual behavior, and eating.

Duopa is an intestinal gel formulation of the carbidopa-levodopa combo that AbbVie developed to help manage Parkinson’s symptoms. It reduces the time when standard levodopa treatment wears off — periods known as off times.

Little is known about its non-movement side effects, however.

Spanish researchers wanted to know if Duopa would increase impulse control disorders in Parkinson’s patients. Their study involved 62 patients with an advanced form of the disease who received Duopa for six months. The patients had had symptoms a median of 13.5 years and movement problems a median of five years.

Duopa reduced patients’ off periods by almost six hours a day, or 79 percent. It failed to reduce the duration of patients’ uncontrolled movements, however. Duopa also improved patients’ ability to perform daily activities. In general, the treatment reduced the severity of the disease’s symptoms by 25 percent.

The treatment also led to signficant improvements in patients’ scores on an impulse control disorder index known as the Questionnaire for Impulsive–Compulsive Disorders in Parkinson’s disease. Patients’ scores fell by 54 percent over three months and by 64 percent over six months.

In terms of type of disorder, there were significant reductions in compulsive eating, in taking medication compulsively, in becoming compulsive hobby enthusiasts, and in compulsive punding, or engaging in repetitive mechanical tasks like assembling and disassembling things.

In contrast, Duopa led to no changes in compulsive gambling, sex, or buying.

Another finding was that the therapy led to significant reductions in psychosis, improved sleep quality and better social interactions.

“Currently, there is no consensus regarding treatment of impulse control disorders,” the researchers wrote. Key reasons are the variability of impulsive behavior symptoms and lack of clinical trials addressing the issue, they said.

As a whole, the study indicated that Duopa could be a good way to help people with advanced Parkinson’s disease manage their impulse control disorders.

Importantly, Duopa can significantly improve patients’ movement symptoms and sleep quality without a significant increase in levodopa dosage, the researchers wrote.

But additional studies are necessary to compare Duopa’s impact with that of other commonly used Parkinson’s treatment, the team added.

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The Old Me Versus the New Me

 

Sherri Journeying Through

I used to be happy. I used to be a lot of fun. Or, so I’ve been told.

What happened to me? The me who used to not have to take pills to feel good? The me who used to laugh all the time with others and dance all the time with my kids, and sing all the time at the top of my lungs? The me who even I liked?

My kids have told me they want their “old mom” back. How can I give them what was stolen? How can I get back what was taken away — involuntarily, I might add?

I try to stay “up,” try to keep a positive attitude, a joyous spirit. But it’s positively a hard thing to do when this thing — this monster called Parkinson’s disease — continually insists on having its way. Every time I start feeling as if the “old me” is making a comeback, the “new me” butts in.

Sometimes, I don’t have a choice in this transition; this changing of life. Sometimes, I don’t get to choose the up days from the down days, and the in-between days from the lost days. Sometimes, the bad days really are as bad as they seem and the good days are really better than it appears. It’s a big game this little monster plays: deceiving you, deceiving me.

I’m going to try — try real hard — to hold on to the old me. The one before the pills. The me before I got lost. The me that used to laugh all the time, danced with my kids all the time, sang all the time. I am going to try to hold on to the old me, despite the color of my hair. (Of which I earned each and every gray strand by being a mom while being the old me.)

I’m going to try to be up when I’m down and not cry when I feel like crying … over lost things. And if I can’t summon up the old me while living the new me, please don’t give up on whoever I am, because the old me really is alive struggling to be loose, let out, set free.

***

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.

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Acorda Asks European Union to Approve Inbrija for Parkinson’s Off Periods

Inbrija approval request

Acorda Therapeutics has asked the European Medicines Agency to approve Inbrija (CVT-301) to reduce the periods when the standard Parkinson’s treatment carbidopa/levodopa is not working.

Inbrija is a self-administered, inhaled levodopa therapy. Acorda developed it to reduce the time when standard levodopa treatment wears off — periods known as off times.

Both movement and non-movement symptoms return during off times. About half of  patients taking standard levodopa have off periods, which become more frequent and severe during the course of the disease.

Inbrija was designed to deliver a precise dose of a dry powder form of levodopa to patients’ brains. The powder form bypasses the digestive system, preventing delays in the medication kicking in.

Acorda filed a marketing authorization application asking the European Union to approve the therapy. The application included results from its 12-week Phase 3 SPAN-PD clinical trial (NCT02240030). The study assessed the safety and effectiveness of 84-mg and 60-mg doses of Inbrija’s administered up to five times a day in 351 Parkinson’s patients experiencing off periods.

Inbrija improved patients’ movement in comparison with a placebo, results showed.

In line with a previous Phase 2b trial, researchers found no lung safety concerns. The most common adverse events were cough, upper respiratory tract infection, and throat irritation.

Acorda presented the SPAN-PD results at the International Congress of Parkinson’s Disease and Movement Disorders in Vancouver, Canada, in June 2017.

The application included the results of two long-term Phase 3 safety trials as well. The CVT-301-005 trial (NCT02352363) covered 408 patients, and the CVT-301-004E study (NCT02242487) 325 participants.

Researchers found no changes in the treated patients’ lung function, compared with standard levodopa treatment. Taken together, the findings indicated that Inbrija was safe as an off-period treatment, Acorda said.

The U.S. Food and Drug Administration accepted Acorda’s New Drug Application for Inbrija in February 2018. It expects to decide by October 5 whether to approve it.

U.S. regulators refused to accept Acord’s initial application due to concerns over the manufacturing of Inbrija. The company addressed the questions in a revised application.

Acorda’s European application covers all European Union countries, as well as Norway, Liechtenstein, and Iceland.

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Protein Mediates Nerve Cells’ Susceptibility to Neurotoxins, Mouse Study Finds

AQP9 dopaminergic neurotoxins

A protein found on the surface of cells mediates nerve cells’ susceptibility to damage and death. This discovery may open new therapeutic avenues to prevent neuron degeneration associated with Parkinson’s disease.

The study, “Targeted deletion of the aquaglyceroporin AQP9 is protective in a mouse model of Parkinson’s disease,” was published in PlosOne. 

Only 10 percent of Parkinson’s disease cases are associated with an inherited genetic cause, and it is still unclear what causes the remaining 90 percent of all sporadic cases. External, environmental toxins are believed to play a role in the development of Parkinson’s disease, but it is not known why dopaminergic neurons are more susceptible to damage.

Previous studies have shown that a protein called AQP9, is present in the dopaminergic neurons of of rats’, mice, and primates’ substantia nigra, which is the brain area affected in Parkinson’s disease and responsible for control movement and coordination.

This particular protein regulates cellular permeability and is an important mediator of cells’ contact with their exterior environment.

University of Oslo researchers evaluated the role of AQP9 in mediating cells’ response to Parkinson’s associated toxins.

They tested AQP9-positive cells’ permeability to MPP+ — a neurotoxin known to selectively affect dopamine neurons — and found that MPP+ transport was twofold higher in AQP9-positive cells than in any other cell.

To evaluate the role of AQP9 in MPP+-mediated toxicity on dopaminergic neurons, the team used brain slices collected from the substantia nigra of mice that had been genetically engineered to lack AQP9. When exposed to the neurotoxin the number of dopamine-producing cells remained roughly the same. In contrast, dopamine producing cells from normal mice died, a response that was prevented upon treatment with an AQP9 inhibitor.

The production of dopamine and dopamine-derived molecules was less affected in mice that did not have the AQP9 protein, suggesting they are, to some extent, protected from MPP+‘s harmful effects.

“Our data open for the possibility that toxins and other parkinsonogenic substances access dopaminergic neurons through AQP9,” the researchers stated.

These findings suggest that this surface protein should be explored as a new target for pharmacological intervention.

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New Scanner Worn as Helmet Allows Brain Imaging in Parkinson’s Patients

brain imaging

A new brain scanner that can be worn as a helmet could potentially revolutionize the world of human brain imaging, allowing patients with Parkinson’s disease to undergo brain scanning — a task previous traditional scanners failed.

Brain cells use electrical impulses to communicate and, in doing so, form small magnetic fields that can be detected outside the head. Human brain function can be imaged by capturing these magnetic fields through a technique called magnetoencephalography (MEG).

With current scanners, patients have to remain perfectly still while being scanned, as even a tiny movement could render the images unusable. This means it is very difficult to scan people who find it hard to remain still, such as patients with movement disorders.

Researchers at the Sir Peter Mansfield Imaging Centre, University of Nottingham UK have tackled this issue by developing a new MEG system that’s worn as a helmet, allowing subjects to move around freely and naturally during scanning.

The new scanner is more sensitive than current systems, giving a detailed, millisecond-by-millisecond picture of the brain while subjects perform different tasks, such as speaking or moving.

It was recently described in the study, “Moving magnetoencephalography towards real-world applications with a wearable system,” published in the journal Nature.

“This new technology raises exciting new opportunities for a new generation of functional brain imaging. Being able to scan individuals whilst they move around offers new possibilities, for example to measure brain function during real world tasks, or genuine social interactions. This has significant potential for impact on our understanding of not only healthy brain function but also on a range of neurological, neurodegenerative and mental health conditions,” Matt Brookes, PhD, the study’s co-lead author, said in a press release.

Traditional scanners are extremely heavy, weighing about half a ton, because their sensors require extremely low temperatures (-269 degrees Celsius, equivalent to -452 degrees Fahrenheit), which means the machine must contain built-in cooling technology.

The new scanner has scaled-down technology that takes advantage of “quantum” sensors incorporated in a 3-D printed prototype helmet. The new sensors are extremely lightweight and can work at room temperature, allowing them to be placed directly onto the patient’s head. This positioning also means the sensors are closer to the brain, increasing the amount of signal they can pick up.

To allow patients to move their heads during scanning, researchers had to adjust the helmet’s electromagnetic potential and build special electromagnetic coils.

After designing a successful prototype, researchers are now developing new types of helmets to fit babies and children, as well as adults. They predict this new type of scanner will increase the sensitivity of brain imaging fourfold in adults, and up to 15 or 20 times in children.

“This has the potential to revolutionize the brain imaging field, and transform the scientific and clinical questions that can be addressed with human brain imaging. Our scanner can be worn on the head like a helmet, meaning people can undertake tasks whilst moving freely. Importantly, we will now be able to study brain function in many people who, up until now, have been extremely difficult to scan — including young children and patients with movement disorders. This will help us better understand healthy brain development in children, as well as the management of neurological and mental health disorders,” said Gareth Barnes, PhD, a professor and the leader of the project at Wellcome Centre for Human Neuroimaging at University College London.

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‘PATH to PD’ Program Seeks to Deepen Understanding of Parkinson’s Onset, Progression

Michael J. Fox Foundation

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) will fund a new program to investigate the pathogenesis of Parkinson’s disease called “PATH to PD.”

The two-year program includes three research teams that will collaborate to investigate risks associated with genetics, environment and aging, while working with a common framework to gain a better understanding of the onset and progression of Parkinson’s.

Each PATH to PD-funded project will receive $2 million.

“The vast diversity of pathways implicated in Parkinson’s pathology to date indicates that multiple physiological routes can lead to PD, and these routes may intersect or be temporally dependent,” Todd Sherer, PhD, CEO of MJFF, said in a press release. “Through PATH to PD, our Foundation aims to encourage researchers to bring a holistic new approach to bear on refining today’s understanding of what Parkinson’s is — so that we can better strategize how to slow or stop the disease.”

Parkinson’s is not fully understood by scientists. Even though it is known the disease stems from gene-environment interactions as we age, the emerging picture of Parkinson’s is that of a vast, interwoven network culminating in a disease that varies greatly in cause, rate of progression, symptomology and treatment response.

All three teams will collaborate to build a common framework linking mechanisms through which genetics, environment and aging-associated risk and causal factors may lead to Parkinson’s disease.

University of Pittsburgh researchers, led by J. Timothy Greenamyre, MD, PhD, will seek out links between environmental and genetic triggers of the disease. Researchers will look into the mechanisms that lead neurotoxins to cause neurodegeneration and how these pathways are involved in interactions with genetic factors such as LRRK2 (leucine-rich repeat kinase 2), the leading genetic cause of the disease.

National Institutes of Health researchers, led by Andrew Singleton, PhD, will map the genetic effects in Parkinson’s by growing nerve cells from induced pluripotent stem cells, and map how various genetic alterations lead to the molecular and cellular changes associated with Parkinson’s.

Northwestern University researchers, led by D. James Surmeier, PhD, will investigate the link between aging and Parkinson’s. Using advanced gene-editing techniques, they will look at how cellular aging and related DNA and mitochondrial damage contribute to neurodegeneration in rodent and human cells.

These efforts have the common goal of developing a disease-modifying treatment for Parkinson’s disease, so that it can stop or slow disease progression.

For disease-modifying treatments to work best, however, they should target key underlying disease-causing pathways, which need to be identified and isolated first.

Some cases of Parkinson’s occur due to genetic factors, known as familial Parkinson’s disease. However, familial Parkinson’s is only a small fraction of all diagnoses of the disease. Informed guesses lean toward  environmental factors, including heavy metal or pesticide exposure, since aging still accounts for the greatest risk factor underlying this disease.

The fact that there is no identifiable cause of immediate contamination, researchers suspect this might be due to a lifetime accumulation of otherwise minor compound exposures that eventually lead to the development of the disease or contribute to a “switch” in Parkinson’s risk genes. Perhaps the process occurs naturally as medicine allows us to live longer, or perhaps it’s a combination of both.

“With Parkinson’s prevalence expected to double by 2040 to nearly 13 million people worldwide, our Foundation believes it is our obligation to continue building on current research momentum to eradicate this disease once and for all,” Sherer added.

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What Deep Brain Stimulation Can and Can’t Do

DBS

 

We sometimes don’t get all of our facts straight when it comes to pursuing what we want. As Parkinson’s patients, we only want one thing: a cure. Since we know that a cure is being researched but we don’t know when it will come about, we are grateful for anything that comes along in the meantime.

While that “anything” may not cure us, we’re glad for any way that it helps to make the day-to-day reality of living with Parkinson’s disease easier and more comfortable. This includes things like Sinemet (carbidopa levodopa), a medication that serves as a type of replacement for the missing dopamine in our brains. Or Lexapro (escitalopram), one of those wonder drugs that helps keep us on an even keel, knowing that depression can play a large, often hidden role in Parkinson’s disease, more than most realize.

And then there’s deep brain stimulation (DBS). The National Institute of Neurological Disorders and Stroke describes the treatment as follows:

DBS “is a surgical procedure used to treat a variety of disabling neurological symptoms—most commonly the debilitating symptoms of Parkinson’s disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems. At present, the procedure is used only for patients whose symptoms cannot be adequately controlled with medications.”

It “uses a surgically implanted, battery-operated medical device called a neurostimulator—similar to a heart pacemaker and approximately the size of a stopwatch—to deliver electrical stimulation to targeted areas in the brain that control movement, blocking the abnormal nerve signals that cause tremor and PD symptoms.”

DBS has proven to do more than someone with Parkinson’s disease could have hoped for. But sometimes we forget the facts and hope for so much more. We may forget that DBS isn’t a cure as we come away from the surgery. We’re feeling great after our stimulator has been activated. The tremors have ceased or at least eased. We are getting by with lower amounts of medication. We may not be as stiff or rigid. We can move with less struggle and walk with more confidence.

However, perhaps we seem to be feeling slightly more depressed. Perhaps we’re having trouble finding our “words,” and when we do find them, we struggle to get them out. If only one side of our brain was “stimulated,” perhaps we’re now noticing how the disease seems to have progressed to the other side. But perhaps that side just wasn’t as noticeable prior to the surgery because we were distracted while trying to control the more pronounced side.

There may be more controllable symptoms. There may be less. DBS is not a fix-all. You will still have Parkinson’s when you wake up after surgery, but now it may be an even more “invisible” disease. DBS can control the symptoms. It can give you back so much of what you’ve missed. It seemingly works miracles but it isn’t a cure. Exercise is still vital. Proper medication for the symptoms that DBS doesn’t control (such as depression) need to be monitored regularly.

If you are thinking about having deep brain stimulation, talk to others who have been through it. Read about it. Talk to your doctor and ask every question you can think of. Talk to some more people. If you feel it’s right for you and your doctor supports and recommends the procedure, get the prep work done. If all is a go, then set a date.

However, remember that DBS isn’t a replacement for treatment — it is an extension of well-managed treatment that can enhance your life. If your treatment is not well-managed — medications don’t work well, ons and offs are hit-and-miss, dosages haven’t been updated in a while, etc. — then you probably need to get on track there first.

DBS isn’t a cure, no. But it can make you feel and move a whole lot better. However, you need to remember that what works for one person may not work for another. Parkinson’s disease presents itself differently in each individual, and so each person will respond to treatments differently.

***

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.

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Mutation Can Trigger Parkinson’s Outside the Brain, Study Finds

Parkinson's outside the brain

The most common gene mutation in Parkinson’s triggers disease outside the brain by changing the body’s immune response to common infections, a study in mice reports.

The research, “Mutant LRRK2 mediates peripheral and central immune responses leading to neurodegeneration in vivo,” was published in the journal Brain.

Parkinson’s patients typically lose dopamine nerve cells in a brain area called substantia nigra, resulting in protein clumps known as Lewy bodies and an increase in brain inflammatory cells. In fact, increasing evidence shows that nerve cell inflammation is key to the development of the disease.

“We know that brain cells called microglia cause the inflammation that ultimately destroys the area of the brain responsible for movement in Parkinson’s,” Dr. Richard J. Smeyne, the study’s senior author, said in a press release. “But it wasn’t clear how a common inherited mutation was involved in that process, and whether the mutation altered microglia.”

Only 10 percent of Parkinson’s cases have a genetic cause. Among these, LRRK2 gene cause the most cases. Mutated LRRK2 is found in 15 to 20 percent of Parkinson’s patients who are Ashkenazi Jews patients and in 40 percent of patients who are North African Arab Berbers.

But the precise link between LRRK2 and Parkinson’s remains poorly understood.

“We know that gene mutation is not enough to cause the disease,” said Dr. Elena Kozina, the study’s first author. “We know that twins who both carry the mutation won’t both necessarily develop Parkinson’s.” Another “initiating event,” or hit, is needed, she said.

Smeyne’s team had already observed that a certain strain of influenza virus predisposed mice to develop disease characteristics that mimic Parkinson’s. This prompted them to wonder if a second hit could come from an infection.

The scientists suspected that LRRK2 mutations could be causing effects outside the brain. To test that idea, they used lipopolysaccharide (LPS) — the major component of the outer shell of gram-negative bacteria — to trigger an immune reaction in the mice.

Neither LPS nor the immune cells it activates are able to cross the blood-brain barrier. This gave the team the perfect tool to test whether inflammation on the periphery affects the brain.

They gave LPS to mice with high levels of the two most common LRRK2 gene mutations. LPS triggered a three to five-fold increase in inflammatory regulators, called cytokines, in these mice, compared with control mice and mice with normal LRRK2.

The cytokines were produced by immune T- and B-cells, two types of white blood cells.

Mice with high levels of cytokines also showed enhanced LRRK2 gene expression in certain immune cells and in activated cells of the brain. This led to nerve cell loss in the substantia nigra, a brain area that plays a critical role in movement.

Nerve cell inflammation in these mice may have been triggered by the ability of circulating cytokines to cross the blood-brain barrier and enter the brain, the team said. This could have created an environment that led to the destruction of the substantia nigra and therefore, movement impairment.

”Overall, this study suggests that peripheral immune signaling plays an unexpected — but important — role in the regulation of neurodegeneration in LRRK2-associated Parkinson’s disease, and provides new targets for interfering with the onset and progression of the disease,” the researchers wrote.

Smeyne cautioned that further research is needed to confirm this link and test it in humans. However, “these findings give us a new way to think about how these mutations could cause Parkinson’s,” he said.

“Although we can’t treat people with immunosuppressants their whole lives to prevent the disease, if this mechanism is confirmed, it’s possible that other interventions could be effective at reducing the chance of developing the disease,” Smeyne added.

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Structural Changes in Brain Predict Cognitive Decline in Parkinson’s Patients, Study Suggests

Parkinson's cognitive decline

Structural changes in a specific region of the brain can predict the onset of cognitive impairment in Parkinson’s patients who have not yet developed dementia, according to a recent British study.

The study, “Nucleus basalis of Meynert degeneration precedes and predicts cognitive impairment in Parkinson’s disease,” was published in the journal Brain.

A brain region called the nucleus basalis of Meynert has been identified as the primary source of acetylcholine — a brain chemical important for cognitive function development, including memory, learning, and concentration abilities.

Cognitive impairment is highly prevalent in Parkinson’s disease, with approximately 80 percent of patients eventually developing dementia during the course of their illness. It is one of the most clinically relevant symptoms of the disease, and causes an increased risk of mortality and significant reduction in quality of life.

Studies have demonstrated that the structure of the nucleus basalis of Meynert appears to be more damaged in Parkinson’s patients with cognitive impairment. However, so far, there are no reliable predictors of dementia in Parkinson’s, and the mechanisms behind the development of cognitive impairment remain unclear.

King’s College London researchers hypothesized that structural changes in this specific brain region could be behind cognitive impairment in patients with Parkinson’s disease, and could predict the development of cognitive impairment. To test this, the team compared magnetic resonance imaging (MRI) data from Parkinson’s patients with and without cognitive impairment.

A total of 304 Parkinson’s patients and 167 healthy people in a control group were included in the study. The participants’ cognitive status was assessed at the start and then every six months for 36 months, or until a patient developed cognitive impairment.

No brain anatomy differences were observed between Parkinson’s patients and the control group. However, cognitively impaired patients had higher rates of neuronal loss within the nucleus basalis of Meynert than non-demented patients with Parkinson’s.

Damage to this brain region “was predictive for developing cognitive impairment in cognitively intact patients with Parkinson’s disease, independent of other clinical and non-clinical markers of the disease,” the authors wrote.

The team also analyzed the anatomy of other cognitive function-related brain centers, but structural and microstructural changes to those regions did not precede clinical onset of cognitive impairment.

Researchers concluded that “degeneration of the nucleus basalis of Meynert precedes and predicts the onset of cognitive impairment, and might be used in a clinical setting as a reliable biomarker to stratify patients at higher risk of cognitive decline.”

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