Understanding and Managing PD-Related Shame and Embarrassment

Friday October 17, 2014

Those of us living with PD often experience distressing shame and embarrassment secondary to some of our PD symptoms. When eating in public, for example, hand tremors can cause us to spill food all over the dining table and ourselves. The same tremors plus slowness of movement, have us struggle getting money or credit cards out of our wallets while the cashier, and customers waiting in line, show clear signs of impatience. Excessive salivation can result in drooling. Poor balance makes us walk unsteadily, as if under the influence of alcohol or drugs. The list is not exhaustive.

A good friend of mine who has struggled with PD for the past three years put it this way:

I am embarrassed by my hand shaking, I don’t like the feeling of having little control over such an expressive part of my body. Unfortunately, trying hard to make it stop only seems to make it worse…

 [I feel embarrassment] when gesturing during personal conversations I notice the eyes of my conversational companion move to my tremoring hand…

Embarrassment and shame are powerful emotions that can seriously disrupt our sense of well-being. They heighten our anxiety. They place us at risk for greater distress in the form of social and emotional isolation, and/or psychiatric disorders such as phobias and depression.

We cope with shame and embarrassment in different ways. Typically we keep ourselves in a state of constant alertness wherein we scan the environment for potentially shame-inducing situations and when we spot them we proceed to avoid them. If avoidance is not possible, we anticipate possible obstacles and formulate a solution. We hide symptoms. We dissimulate.

Shame, while frequently encountered by PWP’s, is infrequently discussed. There is irony at play. For many PWPs, it is embarrassing to talk about embarrassments.

The Psychology behind Shame

Viewed from the lens of psychology, cognitively, shame is an emotion that originates from a set of beliefs, namely that one’s body and/or mind are flawed in some significant way; that the presumed defect or stigmata must be kept hidden, secret, away from the scrutiny of others; that to do otherwise exposes the self to public ridicule, scorn or rejection. We fear exposure.

When shame is experienced in public, and it is of mild to moderate intensity, it is known as embarrassment. We feel observed and reproached by others. We blush, we cover our faces, we wish to escape the situation. In its severe form, shame becomes humiliation, and then we wish we had never existed at all.

It appears that the frequency and intensity of felt shame and embarrassment vary; there are individual differences. PWP’s with a premorbid history of self-consciousness, shyness, introversion, interpersonal sensitivity, or socially avoidant behaviors are presumed to be more vulnerable than their extroverted, socially outgoing counterparts.

But living in fear and defending ourselves trough avoidances needs not be our fate.

Coping Effectively with Shame & Embarrassment

A more effective way to cope is to confront the fears head on, with assistance from a psychotherapist trained in Cognitive-Behavioral Therapy (CBT). One helpful technique, among many others, is that of behavioral exposure to the paralyzing fear. The idea is that the client engages in an activity that brings on the fear of embarrassment and in doing so, and working through it, learns that the situation is not devastating. When combined with other CBT techniques, such as cognitive restructuring, thought stopping, disputing the inner critic, relaxation techniques, mindfulness training, such forms of behavioral exposure can result in lasting changes. Practical advice: Discuss your fears with your health team and obtain a referral for CBT with a trained therapist.

But psychotherapy is not for everyone.  Some PWP’s might  prefer to enlist the help of a life coach  who will assist the PWP with the formulation and implementation of  behavioral goals and objectives that are antidotes to fear—like courage, for example. Practical advice: Access a reputable website on coaching and positive psychology, such as www.positiveacorn.com

It might also be the case that the PWP prefers self-management or self-help efforts. This can be effective too, provided that the recommended interventions are evidence based.  The work involved, as with coaching, focuses on designing and implementing goals, but the coach is you.

Effects of high-risk Parkinson's mutation are reversible

Oct.16,2014

Researchers from the University of Sheffield have found vital new evidence on how to target and reverse the effects caused by one of the most common genetic causes of Parkinson's.

Mutations in a gene called LRRK2 carry a well-established risk for Parkinson's disease, however the basis for this link is unclear.

The team, led by Parkinson's UK funded researchers Dr Kurt De Vos from the Department of Neuroscience and Dr Alex Whitworth from the Department of Biomedical Sciences, found that certain drugs could fully restore movement problems observed in fruit flies carrying the LRRK2 Roc-COR Parkinson's mutation.

These drugs, deacetylase inhibitors, target the transport system and reverse the defects caused by the faulty LRRK2 within nerve cells. The study is published in Nature Communications.

Dr De Vos, a Lecturer in Translational Neuroscience at the world-leading Sheffield Institute for Translational Neuroscience (SITraN), said: "Our study provides compelling evidence that there is a direct link between defective transport within nerve cells and movement problems caused by the LRRK2 Parkinson's mutation in flies."

Co-investigator Dr Alex Whitworth explained: "We could also show that these neuronal transport defects caused by the LRRK2 mutation are reversible.

"By targeting the transport system with drugs, we could not only prevent movement problems, but also fully restore movement abilities in fruit flies who already showed impaired movement marked by a significant decrease in both climbing and flight ability." 

The LRRK2 gene produces a protein that affects many processes in the cell. It is known to bind to the microtubules, the cells' transport tracks. A defect in this transport system has been suggested to contribute to Parkinson's disease. The researchers have investigated this link and have now found the evidence that certain LRRK2 mutations affect transport in nerve cells which leads to movement problems observed in the fruit fly (Drosophila).

The team then used several approaches to show that preventing the association of the mutant LRRK2 protein with the microtubule transport system rescues the transport defects in nerve cells, as well as the movement deficits in fruit flies.

Dr De Vos added: "We successfully used drugs called deacetylase inhibitors to increase the acetylated form of α-tubulin within microtubules which does not associate with the mutant LRRK2 protein. We found that increasing microtubule acetylation had a direct impact on cellular axonal transport.

"These are very promising results which point to a potential Parkinson's therapy. However, further studies are needed to confirm that this rescue effect also applies in humans."

Dr Beckie Port, Research Communications Officer at Parkinson's UK, which helped to fund the study, said: "This research gives hope that, for people with a particular mutation in their genes, it may one day be possible to intervene and stop the progression of Parkinson's. 

"The study has only been carried out in fruit flies, so much more research is needed before we know if these findings could lead to new treatment approaches for people with Parkinson's.

http://www.medicalnewstoday.com/releases/283959.php

Dealing With Parkinson’s Disease-Related Depression

10/14/2014

NPF's National Medical Director, Dr. Michael S. Okun, and Vice President of Research Programs, Peter Schmidt, PhD, comment on Parkinson's and depression in the below article from U.S. News. 

The two conditions go hand in hand.

Depression in Parkinson’s disease patients is a little like the riddle about the chicken and the egg: Which came first – the nervous system disorder characterized by impaired movement and slurred speech, or the depression that is both an early symptom of the disease as well as a consequence of it?

Until a decade or two ago, scientists thought the latter was true, says Michael Okun, a neurologist and co-director of the University of Florida’s Center for Movement Disorders and Neurorestoration. “The prevailing thought was that it was a reactionary thing, like a reaction to a traumatic event,” says Okun, who is also the medical director of the National Parkinson Foundation. “Now we think there are biological changes in the brain that we believe underlie depression.”

In Parkinson’s disease, cells are dying off in certain parts of the brain, creating a deficiency of neurotransmitters that affect our mood. Much of the attention has focused on loss of dopamine, which causes the tremors, slowness and stiffness associated with Parkinson’s. But other neurotransmitters – serotonin and norepinephrine – also undergo “robust degeneration,” Okun says, which is largely responsible for the onset of depression.

Depression as an Early Warning Sign of Parkinson’s 

Depression may predate the onset of motor impairment, and in fact be the first sign of Parkinson’s disease, five to 10 years before a Parkinson’s diagnosis. According to Jim Beck, vice president of scientific affairs at the Parkinson’s Disease Foundation, 60 percent of Parkinson’s disease patients suffer from depression, which preceded Parkinson’s disease for 30 percent.

Spotting depression early can be difficult, since the initial symptoms may be subtle and overlap with Parkinson’s itself, Okun says. Typical symptoms of both conditions include loss of energy and interest in things, as well as overall slowness, both in movements and mental response time. The earlier depression is diagnosed, the better, since “the longer you are depressed, the harder it is to reverse it,” says Peter Schmidt, chief information officer at the National Parkinson Foundation. “If left untreated, the brain will adapt to being depressed. The brain is optimized structurally to do the things that you do.”

Depression in Parkinson’s patients is also “the main driver of quality of life,” Schmidt adds. This result emerged from the Parkinson’s Outcome Project, a survey of more than 7,500 Parkinson’s patients in the U.S., Canada, the Netherlands and Israel. In other words, depression was the top criterion for patients evaluating their own health status.

That may be a stunning revelation, considering the focus of doctor’s visits is normally on the physical degeneration associated with Parkinson’s, Okun says. That’s in part because most Parkinson’s disease patients are only ever treated for their condition by their neurologists – after having been diagnosed by their geriatrician or general practitioner. None of these doctors specialize in psychiatric issues, nor would they necessarily think to refer patients to a psychiatrist, Schmidt adds.

Patients treated at places that refer them to mental health professionals, which is the case largely at academic medical centers like the University of Florida, have the lowest rates of depression, according to the Project results, Schmidt says. “A lot of these centers are helping patients early,” Schmidt says.

Treating Depression and Parkinson’s in Tandem

At UF Health, psychiatrist Herb Ward’s office is down the hall from Okun’s. “We exchange notes on patients,” Ward says. “It’s the best way to do it.”

Ward says he sees patients even more frequently than Okun will, starting with monthly appointments that become quarterly. Ward normally starts treatment plans with antidepressants, which work directly on the neurotransmitters that Parkinson’s depletes. “We can usually choose an agent that is a good fit with the patient,” Ward says, adding that antidepressants’ typical side effects, like weight gain, can actually play in Parkinson’s disease patients’ favor.

“Weight loss is common in Parkinson’s disease, so weight gain can be a good thing,” Ward says, adding that sleep issues are also common. “We can use a sedating antidepressant at night, so the side effect profile isn’t always a negative thing.”

Psychotherapy and cognitive behavioral therapy are also helpful, especially when combined with antidepressants, Ward adds. And for patients who don’t respond to either of these approaches, the more invasive therapies – transcranial magnetic stimulation and electroconvulsive therapy – work well with few side effects, Okun adds.

The key for patients and their caregivers, experts say, is to know if patients are at risk of Parkinson’s disease and related depression and to be proactive about handling both.

“If you have a family history [of Parkinson’s disease] and develop depression at an early age, you should be aware of your risk of Parkinson’s disease,” Schmidt says, adding that people with a history of depression are 2.4 times more likely to develop Parkinson’s disease, even though the percentage of people over age 55 with Parkinson’s is still relatively small at 1.5 percent.

But the sheer prevalence of depression in Parkinson’s patients, coupled with neurologists’ natural preoccupation with treating the disease's physical, rather than psychological, consequences, “puts the onus on patients to be well educated,” Beck says. “Be on the lookout for signs, and speak up to physicians. It’s the kind of conversation that needs to happen.”

And mostly, don’t suffer in silence, he adds. While on a positive note, suicides are rarer among Parkinson’s disease patients than the general population, suicidal thoughts plague many patients chronically. Robin Williams may have been one tragic example of that tendency. He was struggling with the early stages of Parkinson's, which may have exacerbated his struggles with depression. For most Parkinson's patients, however, suicide is not the outcome because the very loss of energy and apathy associated with the disease (symptoms overlapping with depression) are what actually prevent patients from going through with it, Beck says.

“That may be a silver lining, but it’s no way to live life,” Beck says.

— Kristine Crane
Copyright 2014 © U.S. News & World Report LP.

Parkinson: How toxic proteins stress nerve cells

Last updated: 15 October 2014 at 2am PST

Parkinson's Disease is the second most common neurodegenerative disorder. In Germany alone, almost half a million people are affected. The focus of the disease is the progressive degeneration of dopamine-producing nerve cells in a certain region of the midbrain, the substantia nigra. Misfolded proteins are the cause. Until recently, it was unclear why damage is confined to specific nerve cells. A team or researchers led by Frankfurt neurophysiologists has now defined how this selective disease process begins using a genetic mouse model of Parkinson's disease.

The progressive death of a certain type of nerve cells - dopaminergeic neurons - in the substantia nigra causes dopamine deficiency, which is the major cause for the motor deficits in Parkinson patients. Although it is possible to therapeutically compensate the dopamine deficiency for a certain period of time, by e.g. administration of L-dopa or dopamine gonists, these therapies do not stop the progressive death of neurons.

In the last two decades, researchers have identivied gene mutations and toxic protein aggregates to cause neurodegeneration, with protein a-synuclein having an essential role. Until recently, it was unclear why only specific types of nerve cells, such as dopaninergic neurons in the substantia nigra, are affected by this process, while others, also expressing the mutant a-syncuclein such as dopaminergic neurons in the immediate vicinity, survive the disease process with little damage.

The research group led by Dr Mahalakshmi Subramaniam and Prof. Jochen Roeper at the Institute for Neurophysiology at the Goethe University, in collaboration with researchers from Frankfurt's Experimental Neurology Group and from Freiburg University, demonstrated for the first time how sensitive dopaminergic substantia nigra neurons functionally respond to toxic proteins in a genetic mouse model. A mutated a-synculein gene (A53T), which causes Parkinson's Disease in humans, is expressed in the mouse model.

In the current issue of the Journal of Neuroscience, the researchers report that the sensitive dopaminergic substantia nigra neurons respond to the accumulation of toxic protein by significantly increasing the electric activity in the affected mid brain regions. In contrast, the less sensitive, neighboring dopaminergic neurons were not affected in their activity. "This process begins as early as one year before the first deficits appear in the dopamine system, and as such it presents an early functional biomarker that may have future potential for preclinical detection of impending Parkinson's Disease in humans," explains Prof Jochen Roeper. "The potential for early preclinical detection of subjects at risk is essential for the development of neuroprotective therapies."

The Frankfurt group, also identified a regulatory protein, an ion channel, which causes the increase in electric activity and the associated stress in nerve cells in response to oxidative damage. This channel provides a direct new target protein for the neuroprotection of dopaminergic neurons. In brain slices, the dysfunction of this ion channel acting as an "electric brake" for dopamine neurons was reversible just by adding redox buffers. If therapeutic drugs could reduce the channel's redox sensitivity in future mouse models, the death of dopaminergic neurons in the substantia nigra might be prevented. Currently, the researchers are studying whether similar processes occur with other Parkinson genes and in aging itself. "The long-term objective is to investigate the extent to which these results from mice might be transferred to humans," says Roeper.

http://www.medicalnewstoday.com/releases/283893.php

LONG TERM EFFECTIVENESS OF THREE TYPES OF PARKINSON’S MEDICATIONS COMPARED

PARKINSON RESEARCH FOUNDATION

Long Term Effectiveness of Three Types of PARKINSON’S Medications Compared

Treatment of newly diagnosed people with PARKINSON’S DISEASE can pose certain dilemmas for both the physician and the patient.  While levodopa therapy is still considered the “gold standard” and most effective treatment, it may not be the best drug of choice for initial treatment.  And PARKINSON’S patients have sometimes been compared to snowflakes, alike in general similarities, but each person has very unique qualities and symptoms.  So there can be no “one size fits all” standard of treatment.

One ambitious study was undertaken in England to try to establish the long-term effectiveness of several categories of drugs standard in the treatment of PARKINSON’S DISEASE.  They divided their study into three categories, levodopa, dopamine agonists and MAO-B (monoamine oxidase inhibitor type B) inhibitors.  Sinemet is a popular levodopa replacement, ropinerole or pramipexole are dopamine agonists and rasagiline or selegiline are MAO-B inhibitors.  This study was designed to see which class of drug provided the most effective long-term control of PARKINSON’S symptoms based on patient mobility scores and provided the best quality of life for the patient.  Over 1,600 subjects were followed for a 9 year period during this study.

528 subjects were assigned to levodopa, 632 subjects received a dopamine agonist and 460 received an MAO-B inhibitor.  After three years of observation, subjects in the levodopa category performed only slightly better in the mobility tests.  Subjects in the dopamine agonist and MAO-B categories mobility scores were also similarly improved with the MAO-B group reporting a slightly better quality of life.

After seven years, levodopa was still effective, however it provided no increased improvement.  Disease progression remained similar in all three groups, as measured by onset of dementia, institutional admissions or death.  28% of the subjects in the dopamine agonist group discontinued the use of the agonists due to side effects.  23% of the group of MAO-B subjects also experienced side effects that caused them to discontinue that medication.   Only 11% of the levodopa group discontinued that treatment due to side effects.

The study authors report that MAO-B inhibitors are as effective as dopamine agonists, but levodopa has a slight edge in improving mobility scores.

PD MED Collaborative Group; Long-term effectiveness of dopamine agonists and monoamine oxidase B inhibitors compared with levodopa as initial treatment for Parkinson’s disease (PD MED): a large, open-label, pragmatic randomised trial; The Lancet, Early Online Publication, 11 June 2014, doi:10.1016/S0140-6736(14)60683-8

Review by Marcia McCall

Why A Care Team?

The Michael J. Fox Foundation for Parkinson's Research shared a link.

3 hours ago

A physical therapist can help you build strength, improve mobility and manage pain.

WHY A CARE TEAM?

Establishing a comfortable, open and productive relationship with your health care providers is important for your overall care. Different patients work with different types of doctors to manage their Parkinson’s: some choose to be treated by a movement disorder specialist; some work with a general neurologist; some stay with their primary care physician. In choosing any health care provider, your major considerations should be how much they know about Parkinson’s and how well they listen.

Because Parkinson’s involves a wide range of symptoms including movement- and non-movement-related issues, over the course of your life with Parkinson’s you may wish to work with a variety of health care providers in addition to the doctor who primarily treats your Parkinson’s. For example, depending on the particular range of symptoms, some patients may find it helpful to include a physical therapist to help address painful muscle stiffness, or a therapist who can provide strategies for coping with depression. Whether over time or for brief periods, working with a team of providers (sometimes called “allied care providers”) in addition to your physician can help you better manage your Parkinson’s care. 

It’s been shown that early involvement by other health care professionals such as an occupational or speech therapist may help prevent or delay future limitations that can be caused by Parkinson’s disease. These relationships can help you manage your functionality and maintain a safe environment as your Parkinson’s progresses. 

It is crucial for any provider to understand that no two cases of Parkinson’s are alike, and to listen to you about your specific concerns. The right doctor will take the time to discuss your symptoms and how they impact you and recommend a treatment regimen with you in mind.

https://www.partnersinparkinsons.org/parkinsons-care-team?cid=smc_fb_000097

Dealing With Parkinson’s Disease-Related Depression

The two conditions go hand in hand.

Knowing the symptoms and being proactive can help patients and caregivers manage Parkinson’s disease and depression.

By Kristine Crane
Oct. 14, 2014 | 11:26 a.m. EDT

Depression in Parkinson’s disease patients is a little like the riddle about the chicken and the egg: Which came first – the nervous system disorder characterized by impaired movement and slurred speech, or the depression that is both an early symptom of the disease as well as a consequence of it?
Until a decade or two ago, scientists thought the latter was true, says Michael Okun, a neurologist and co-director of the University of Florida’s Center for Movement Disorders and Neurorestoration. “The prevailing thought was that it was a reactionary thing, like a reaction to a traumatic event,” says Okun, who is also the medical director of the National Parkinson Foundation. “Now we think there are biological changes in the brain that we believe underlie depression.”
In Parkinson’s disease, cells are dying off in certain parts of the brain, creating a deficiency of neurotransmitters that affect our mood. Much of the attention has focused on loss of dopamine, which causes the tremors, slowness and stiffness associated with Parkinson’s. But other neurotransmitters – serotonin and norepinephrine – also undergo “robust degeneration,” Okun says, which is largely responsible for the onset of depression.

Depression may predate the onset of motor impairment, and in fact be the first sign of Parkinson’s disease, five to 10 years before a Parkinson’s diagnosis. According to Jim Beck, vice president of scientific affairs at the Parkinson’s Disease Foundation, 60 percent of Parkinson’s disease patients suffer from depression, which preceded Parkinson’s disease for 30 percent.
Spotting depression early can be difficult, since the initial symptoms may be subtle and overlap with Parkinson’s itself, Okun says. Typical symptoms of both conditions include loss of energy and interest in things, as well as overall slowness, both in movements and mental response time. The earlier depression is diagnosed, the better, since “the longer you are depressed, the harder it is to reverse it,” says Peter Schmidt, chief information officer at the National Parkinson Foundation. “If left untreated, the brain will adapt to being depressed. The brain is optimized structurally to do the things that you do.”
Depression in Parkinson’s patients is also “the main driver of quality of life,” Schmidt adds. This result emerged from the Parkinson’s Outcome Project, a survey of more than 7,500 Parkinson’s patients in the U.S., Canada, the Netherlands and Israel. In other words, depression was the top criterion for patients evaluating their own health status.
That may be a stunning revelation, considering the focus of doctor’s visits is normally on the physical degeneration associated with Parkinson’s, Okun says. That’s in part because most Parkinson’s disease patients are only ever treated for their condition by their neurologists – after having been diagnosed by their geriatrician or general practitioner. None of these doctors specialize in psychiatric issues, nor would they necessarily think to refer patients to a psychiatrist, Schmidt adds.  
Patients treated at places that refer them to mental health professionals, which is the case largely at academic medical centers like the University of Florida, have the lowest rates of depression, according to the Project results, Schmidt says. “A lot of these centers are helping patients early,” Schmidt says.

[Read: Coping With Depression at Work]

Treating Depression and Parkinson’s in Tandem
At UF Health, psychiatrist Herb Ward’s office is down the hall from Okun’s. “We exchange notes on patients,” Ward says. “It’s the best way to do it.”
Ward says he sees patients even more frequently than Okun will, starting with monthly appointments that become quarterly. Ward normally starts treatment plans with antidepressants, which work directly on the neurotransmitters that Parkinson’s depletes. “We can usually choose an agent that is a good fit with the patient,” Ward says, adding that antidepressants’ typical side effects, like weight gain, can actually play in Parkinson’s disease patients’ favor.
“Weight loss is common in Parkinson’s disease, so weight gain can be a good thing,” Ward says, adding that sleep issues are also common. “We can use a sedating antidepressant at night, so the side effect profile isn’t always a negative thing.”
Psychotherapy and cognitive behavioral therapy are also helpful, especially when combined with antidepressants, Ward adds. And for patients who don’t respond to either of these approaches, the more invasive therapies – transcranial magnetic stimulation and electroconvulsive therapy – work well with few side effects, Okun adds.

The key for patients and their caregivers, experts say, is to know if patients are at risk of Parkinson’s disease and related depression and to be proactive about handling both.
“If you have a family history [of Parkinson’s disease] and develop depression at an early age, you should be aware of your risk of Parkinson’s disease,” Schmidt says, adding that people with a history of depression are 2.4 times more likely to develop Parkinson’s disease, even though the percentage of people over age 55 with Parkinson’s is still relatively small at 1.5 percent.
But the sheer prevalence of depression in Parkinson’s patients, coupled with neurologists’ natural preoccupation with treating the disease's physical, rather than psychological, consequences, “puts the onus on patients to be well educated,” Beck says. “Be on the lookout for signs, and speak up to physicians. It’s the kind of conversation that needs to happen.”
And mostly, don’t suffer in silence, he adds. While on a positive note, suicides are rarer among Parkinson’s disease patients than the general population, suicidal thoughts plague many patients chronically. Robin Williams may have been one tragic example of that tendency. He was struggling with the early stages of Parkinson's, which may have exacerbated his struggles with depression. For most Parkinson's patients, however, suicide is not the outcome because the very loss of energy and apathy associated with the disease (symptoms overlapping with depression) are what actually prevent patients from going through with it, Beck says.

“That may be a silver lining, but it’s no way to live life,” Beck says.

http://health.usnews.com/health-news/patient-advice/articles/2014/10/14/dealing-with-parkinsons-disease-related-depression?

New Study Looks at Gait Dysfunction and Falls in Parkinson’s

FoxFeed Blog

Posted by  Rachel Dolhun, MD, October 13, 2014

Gait instability and falls are among the most debilitating and frustrating symptoms for those with Parkinson’s disease (PD). Unfortunately, they are also often resistant to or only partially responsive to current therapies that work to increase the dopamine lacking in Parkinson’s. Researchers have therefore been considering the role other brain chemicals, including acetylcholine, play in ambulation issues.

Changes in the acetylcholine system have been implicated in Parkinson’s-associated cognitive dysfunction but might also be blamed for imbalance and falls. In a prior study funded by The Michael J. Fox Foundation, brain imaging showed loss of acetylcholine communication between a cluster of cells in the brainstem and other brain regions involved in coordinating movement and maintaining attention. In people with PD, this deficiency was correlated with increased falls and gait slowing. Another study also suggested that a drug that elevates acetylcholine levels may reduce falls.

To further explore the relationship between acetylcholine and movement problems, the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health (NIH), has awarded researchers at the University of Michigan an $11.5 million grant to launch a five-year study.

Scientists will focus their efforts on understanding the acetylcholine system in more detail, parsing out its effect on falls and assessing its responsiveness to a drug ­— Varenicline (Chantix) ­— that targets acetylcholine receptors. This medication is currently available by prescription to aid smoking cessation.

Investigators are hopeful that by delving into an area of Parkinson’s disease research not yet fully explored they will find more effective therapies specifically targeting gait dysfunction and falls.

Though the study is not recruiting yet, interested volunteers can register to be contacted via the University of Michigan Clinical Studies.

Parkinson's disease can migrate from gut to brain, shows research

Published on October 13, 2014 at 10:14 AM Parkinson's disease may start in the gut

Parkinson's disease is strongly linked to the degeneration of the brain's movement center. In the last decade, the question of where the disease begins has led researchers to a different part of the human anatomy. In 2003, the German neuropathologist Heiko Braak presented a theory suggesting that the disease begins in the gut and spreads to the brain. The idea has since, despite vocal critics, gained a lot of ground. Researchers at Lund University in Sweden now present the first direct evidence that the disease can actually migrate from the gut to the brain.

The so-called Braak's hypothesis proposes that the disease process begins in the digestive tract and in the brain's center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.

Researchers at Lund University have previously mapped the spread of Parkinson's in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and "infects" neighboring cells. Professor Jia-Yi Li's research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain's movement center, giving rise to the characteristic movement disorders in Parkinson's disease.

"We have now been able to prove that the disease process actually can travel from the peripheral nervous system to the central nervous system, in this case from the wall of the gut to the brain. In the longer term, this may give us new therapeutic targets to try to slow or stop the disease at an earlier stage", says Professor Jia-Yi Li, research group leader for Neural Plasticity and Repair at Lund University.

The research team will now carry out further studies in which the mechanisms behind the transport of the harmful protein will be examined in detail. The current study suggests that the protein is transferred during nerve cell communication. It is at this point of interaction that the researchers want to intervene in order to put a stop to the further spread of the disease.

Source:

http://link.springer.com/article/10.1007/s00401-014-1343-6