Welcome to Our Parkinson's Place
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 diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.
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Saturday, October 18, 2014
Thursday, October 16, 2014
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.
Wednesday, October 15, 2014
Tuesday, October 14, 2014
A physical therapist can help you build strength, improve mobility and manage pain.
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.
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.
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.
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.
“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.
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.