March 18, 2017
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.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
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Saturday, March 18, 2017
March 18, 2017
NSW Nationals senator John 'Wacka' Williams has revealed he was diagnosed with Parkinson's Disease last year.
NSW Nationals Senator John 'Wacka' Williams has revealed he was diagnosed with Parkinson's Disease last year.
March 18, 2017
Former Balbriggan mayor, Frank Snowe talks to John Manning about living with Parkinson's and why he's decided to parachute from an aeroplane
Former Balbriggan Mayor Frank Snowe is preparing to do a parachute jump in Perth
A former Mayor of Balbriggan is preparing to parachute from a plane at the age of 65 to raise money and awareness for Parkinson's disease, a condition he was diagnosed with 16 months ago.
Frank Snowe is a well known former Balbriggan town councillor and wore the town's mayoral chain for a year as the Cathaoirleach of that council but for the last couple of years, Frank has been waging a private battle with Parkinson's disease and now he wants to help other people with the same condition.
Frank has found a lack of information and support in the area for people suffering with Parkinson's with the nearest support groups for the condition meeting as far away as Dundalk and Malahide. The former Balbriggan mayor now wants to set up a new support group serving people affected by Parkinson's in Balbriggan and Drogheda, and any point in between.
To that end, he's decided to raise some cash and publicity for his new mission by jumping out of a plane in Australia along with his granddaughter.
When we meet, Frank who was always know for his one-liners, joked about the adventure, saying: 'Well, I decided if I'm shaking all the time, I might as well have a good reason to shake.'
Explaining how the skydive idea came about, he said: 'The idea came from my granddaughter. My son-in-law in Australia did a sky jump about three years ago and his daughter, my granddaughter wanted to do it with him but she was only 10 or 11 but you had to be at least 12 to legally do it.
'So, she was over here on holidays in September and I told her I was going over there (to Australia) and she said to me, well are we going to do the sky jump because I promised her when she was 12 that we could do it.
'So, I said OK, never really thinking we would do it until I got a phone call a couple of weeks ago and Emma (Frank's granddaughter) said she can't wait for me to go over so we can jump out of a plane - so we're going for it.'
Since being diagnosed in November of 2015 with Parkinson's, Frank has found access to information and support difficult. He said: 'I've been a little disappointed with how Parkinson's is dealt with here. You are told by a doctor you have Parkinson's and maybe you can't see a specialist for 12 or 15 months so what do you do? You look up Google or whatever because there's nothing else there for you. In fairness, to the Parkinson's Association of Ireland, they do their best and I wouldn't knock them at all but they haven't really got the funding they need.'
That is why, the money raised by Frank's sky dive will help establish a local support group with the help of the association.
Frank explained: 'I put two and two together and decided that along with doing the jump in Australia, I would do some fundraising for Parkinson's and see if I could possibly help anybody else in the area in Drogheda or in Balbriggan who have Parkinson's and set up something locally and link in with the association.'
The former Balbriggan Mayor believes there is a lot of ignorance among the general population about what living with Parkinson's involves and he is anxious to explain how the condition affects his daily life. One of the most difficult challenges he has faced in dealing with the condition is its impact on his mental and emotional health.
He explained: 'Every week I go to a certain pub in Balbriggan and meet two pals of mine. To be honest, it's not out of choice - I'm sent out.
'One of the things about Parkinson's is that you become a bit antisocial. My missus insists I go down and when I get down there, I do enjoy it but the thoughts of going out and meeting people kills me. I don't know why.'
Frank added that before he was diagnosed: 'I had mood swings and terrible depression without any reason to feel depressed - I would sit at the window and just stare into space and people would come to visit and tell me I was in bad form and what's wrong with me and I'd say 'nothing'.'
The difficult with the condition is that it is hard to recognise in its early days until it physically manifests itself with the familiar tremors.
Frank explained: 'You are told you have Parkinson's when you develop tremors and there's no test for it up to that point but there are 10 early signs of it that you wouldn't know to look for unless you already suspected you had Parkinson's.
'In the early stages, I had gone some peculiar changes in the last couple of years and I couldn't understand what they were.
'I went from being a very outgoing sort of person who had no problem standing up in front of people and speaking publicly, to someone who wanted to sit at the back of the room and didn't want to be involved in anything.
'There were simple little signs like I had fallen a couple of times. Walking along, my right leg would stop all of a sudden and I would stumble.
'Personality-wise, I gave up after playing the game all my life since I was a kid and loving it - I just walked off the course one day and never went back and felt total apathy about it.'
Some of the physical impacts of the condition were first noticed by Frank's wife of more than 40 years. As the couple walked hand-in-hand, she noticed Frank's arm would sometimes stiffen. These and other clues eventually led to medical investigations and then a diagnosis.
Frank remembers receiving that initial diagnosis: 'She (the doctor) said: 'Frank, what did Doctor Google have to say about this?' And I told her: 'Dr Google said it's probably Parkinson's.' And she said: 'Unfortunately, I think Dr Google is right.'
The former Balbriggan town councillor said: 'It made sense of all the things that had been happening to me over the course of a couple of years and explained why I'd felt depressed and all of that so although it came as a shock, it also came as a relief that I wasn't going nuts and I was able to name it and then figure out what the hell I do about it.'
But it was after diagnosis, that Frank began to encounter problems with the system here and found a lack of information and support and lengthy waits to see a medical specialist.
He said: 'There was an appointment made for me to see a specialist in Beaumont in November of 2015 and I finally got to see the specialist in January of this year.'
Frank wants to make those early days of diagnosis a little easier for people in the Drogheda and Balbriggan area by providing a support network for people with the condition that not only provides the necessary information and support in those early stages but also provides continued support for people as the disease inevitably progresses.
In that mission, Frank has taken some inspiration from his nephew, Keith Duffy and his determined charity work for autism. Frank said: 'He gave me the idea to try to turn something bad into something positive and useful.'
He added: 'In a year's time I would like to see people who are out there and in the same boat as I am and have nobody to talk to about it, they have a place to go. Unless you have Parkinson's it is very difficult to describe what it is like and maybe we can help a few people.
'I've built up contacts over the years and I'm fairly good at organising things and know how to chair a meeting so maybe I can use some of those skills to help.'
Asked about his own attitude to the disease, he said determinedly: 'Live with it, get on with it and don't let it beat me - that's my attitude to it. But I know that is very hard to do.
'As time goes on I've got better at dealing with it and this parachute thing and the idea of setting up the group has given me a goal to reach for. It gives me a mission.'
To people who are newly diagnosed with Parkinson's, Frank has some simple but insightful advice. He said: 'If you are newly-diagnosed, I would say first, don't panic. Don't panic and don't keep it to yourself and don't be embarrassed about it.'
The former Mayor said that anyone interested in joining a new support group for people affected by Parkinson's disease from the Balbriggan and Drogheda area, you can contact him by email at firstname.lastname@example.org
If you want to donate to his skydive challenge, go to https://give.everydayhero.com/ie/frank-snowe-charity-sky-dive
Friday, March 17, 2017
March 11, 2017 Steven T. DeKosky, MD; Sam Gandy, MD
Over the past 3 decades, the focus on the molecular pathogenesis of Alzheimer disease (AD) has led to remarkable advances in our understanding of the emergence of symptoms and the course of the disease.
Biomarkers derived from growing knowledge of the pathobiology have enabled identification of amyloid plaques in both symptomatic and cognitively normal individuals, the latter potentially identifying a population at high risk for dementia. About 20 genes have been identified as being associated with increased or decreased risk for late-onset AD (LOAD). Most of these linked genes have been identified by genome-wide association studies and meta-analyses. Each new gene linked to LOAD fills in another gap in our understanding of AD pathogenesis and also serves as a new potential therapeutic opportunity.
Each of the 20 LOAD genes exerts only a small effect on risk. The exception is the apolipoprotein E (APOE) ε4 allele, identified by linkage studies to a site on chromosome 19 and characterized with studies showing binding of the amyloid-β (Aβ) peptide to cerebrospinal fluid proteins. Apolipoprotein E is by far the most prevalent and potent LOAD genetic risk factor yet discovered: each copy of APOE ε4 triples the risk for AD. Additional alleles conferring LOAD risk with anything approaching the power of the ε4 allele are not anticipated based on the prediction that any susceptibility of equal or greater power as compared with APOEε4 surely would have been identified by now.
Despite the advances in genetics and diagnostic markers, the variability in risk and the limited power of allelic risk candidates (beyond APOE ε4) have led increasingly to the conclusion that environmental factors and toxic exposures must also contribute significantly to the risk for developing LOAD. Some of these factors may well exert their actions via newly recognized pathways of DNA methylation and epigenetic modes of influence. The single most compelling piece of relevant data has emerged from the demonstration that monozygotic twins are usually discordant for AD and/or age at symptom onset, providing prima facie evidence for non-genetic modulators. Identification of the important environmental influences that modulate AD risk represents the next great frontier for discovery. Are there smoking guns to be found on this frontier? Is environmental smoke one of them?
At the present time, among the classic (i.e., exogenous) environmental factors, only head trauma has sufficiently robust data to qualify as a widely recognized and currently accepted risk. Polygenic and/or acquired risk factors associated with increased or diminished risk for AD include vascular and metabolic factors (i.e., body mass, blood cholesterol, and blood pressure), glucose homeostasis (i.e., blood glucose and insulin resistance), and exercise. Many of these risks are relevant less at the age at onset of LOAD and more relevant if they have been present in midlife.
The situation in AD contrasts with that in Parkinson disease, another neurodegenerative disorder. 1-Methyl-4-phenyl- 1, 2, 3, 6-tetrahydropyridineandcertain pesticides are now linked convincingly to the risk for Parkinson disease. Among the best known historical associations of environmental toxins with dementing disorders were cycads in Guamanianamyotrophic lateral sclerosis (amyotrophic lateral sclerosis–Parkinson disease complex) and aluminum in AD. However, each of these putative toxin-causing dementia hypotheses has been challenged and, at present, neither is generally accepted to be an authentic association.
The presence of early olfactory and entorhinal pathology in AD has led to speculation that an inhaled agent might be implicated in initiating the disease given (1) the exposure of the olfactory neurons to the environment and their direct connections to the rhinencephalon and (2) the systemic access granted by alveolar entry. Recently, aerosolized vehicular combustion fumes and secondhand smoke have been implicated in both clinical epidemiological and neuropathological studies. Dramatic reports from Calderon-Garciduenas et al revealed diffuse amyloid plaques and inflammation in the brains of children and young adults residing in Mexico City, where the air quality ranks among the worst on the planet.
Transcription of the Alzheimer amyloid precursor protein gene is regulated by acute phase reactant molecules, leading to rapid increases in the levels of amyloid precursor protein and its metabolite Aβ immediately following chemical or traumatic injury. Based on this well-documented phenomenon, one of us (S.G.) examined brain Aβ40 and Aβ42 levels in the brains of mice exposed to an inhaled toxin model of air pollution that used exposure to atmosphere containing aerosolized nickel nanoparticles (NiNPs). Although we expected to see an elevation in brain Aβ following NiNP exposure, we were startled at the rapidity of the effect (i.e., following 3 hours of exposure of the mice to NiNP). This immediate effect was consistent with data reported by one of us (S.T.DeK.) showing rapid elevation and deposition of brain Aβ following severe traumatic brain injury.
Promotion of cerebral amyloidosis is not the only manifestation of inhaled toxin exposure. Davis and colleagues demonstrated important damage to the hippocampal neurons of mice exposed to ambient levels of vehicular aerosols. These and other new frontier studies suggest that many new environmental, genetic, epigenetic, and interaction factors should be explored as a matter of public health stewardship.
In this issue of JAMA Neurology, Richardson and colleagues demonstrated significant elevations of levels of dichlorodiphenyldichloroethylene (DDE), the major metabolite of dichlorodiphenyltrichloroethane (DDT), the common insecticide, in the brains of patients with AD. They also confirmed a strong correlation of serum levels of DDE with brain levels. While the use of DDT has been significantly restricted in the United States for decades (since the environmental damage revealed by Rachel Carson in The Silent Spring), the mean differences in DDE concentrations between AD cases and non-demented control brains were obvious, and some of the DDE levels observed in the AD brains were quite extraordinary.
There are weaknesses in the Richardson et al study, and they are reflective of the typical difficulties in determining environmental risks and/or exposures, especially when exposures occur early in life but clinical manifestations do not appear until many decades later. Issues include (1) variability of the time of and duration of exposures; (2) individuals’ recall of exposures; (3) timing of biological sampling; (4) stability of samples and compounds; (5) proximity of exposure to symptoms (especially of a disorder like AD, where pathological change may develop over decades and subsequent emergence of clinical symptoms is slow and insidious); and (6) how long after exposure the toxic agent (eg, lead in the bones or metabolites in the serum) can be identified. Importantly, variability in the effects of such exposures may also be affected by individual variation in the brain’s reaction to the agent (eg, elevation of amyloid precursor protein and possibly Aβ by DDE, as proposed in this case) and by individual variation in absorption, distribution, metabolism, and excretion of the toxin, as suggested by Richardson et al.
March 17, 2017 by Don Bolser, The Conversation
People with brain diseases, particularly older people, have trouble swallowing. Credit: www.Shutttertock.com
People with brain diseases, particularly older people, have trouble swallowing. Credit: www.Shutttertock.com
Recall that last time you had something "go down the wrong pipe"? You spent the next several minutes coughing, choking and feeling like something bad was in your throat.
It may seem strange to say this, but count yourself lucky.
Your brain was making you do the right things to keep what you drank or ate out of your lungs. The path for air to enter our lungs, the larynx (or voice box), is very close to the upper esophageal sphincter, the entry point for food and liquids to our esophagus. This close anatomical relationship of these two entry points means the brain must coordinate breathing, eating and drinking to ensure the lungs get only air and the esophagus gets only food or liquids. This coordination happens unconsciously, so we never really think about it until we get food or liquid in our airway.
As it turns out, millions of people with brain diseases, including those with Alzheimer's, Parkinson's, Lou Gehrig's disease, stroke, multiple sclerosis and traumatic brain injury, have impaired swallowing. As a result, they are unable to protect their lungs in the way that a healthy person can.
The result is that millions of brain disease patients are at risk for inhaling food and saliva into the lungs, leading to death by pneumonia or even choking.
Detecting and treating impaired swallowing is important, particularly as the nation's nearly 70 million baby boomers continue to age. Impaired swallowing is associated with many conditions of the elderly, and it is often severely underreported. Clinicians may not detect it or may see it as a side effect of another condition.
As a neuroscientist who has studied brain diseases, I know of no pharmaceutical companies that have drug discovery programs aimed at restoring weakened swallow and cough. And yet, it's a major problem.
Hard to swallow, easy to choke
An important part of swallowing is complete closure of the larynx while food is moving through the throat. Disordered swallowing, or dysphagia, limits the ability of the muscles in the mouth and throat to move liquid or food into and through the esophagus and on to the stomach.
This inability to protect the airways and lungs increases the risk of pneumonia or choking.
In addition, many people with brain disorders experience reduced coughing, or a weakened ability to activate breathing muscles to generate airflows that eject material from the lungs. Weakened cough is caused by problems with nerves in our lungs that detect foreign material or with the brain driving the respiratory muscles.
Disordered swallowing can also be caused by problems with nerves in the neck. For example, people who have had cancer of the head or neck often undergo extensive surgery to remove the diseased tissue. This process can inadvertently damage nerves that are important for swallowing.
Sometimes, the swallowing impairment, rather than the primary brain disease, actually leads to death. When swallowing is impaired, it is more likely that material will enter the lungs and trachea during eating or drinking. This is known as aspiration. Aspirated food or drink "seeds" the lungs with material that is coated with pathogens from the mouth. These pathogens are not normally present in the lungs and can cause chronic inflammation and serious bouts of pneumonia.
When a weak cough is a bad sign
In patients with acute stroke, severe swallow and cough impairments occur at the same time. Our research has shown that the risk of aspiration due to swallow impairment can be predicted by weakened cough in patients with stroke or Parkinson's disease. These findings indicate that brain diseases can lead to multiple impairments in how we protect our airways.
Another way of thinking about this problem is that the nervous system has many tools, or reflexes, that it uses to perform certain tasks. Each reflex has a specific function, and the brain coordinates the time of occurrence of each to optimize the result.
For example, a cough can eject material out of the airways into the throat and out of the mouth. Swallows frequently occur just after coughs to move material that was deposited into the throat into the esophagus and then the stomach. The result is that lungs were cleared by coughing, and swallowing moved any remaining material out of the throat to prevent aspiration.
Nearly half of residents of long-term care facilities vulnerable to pneumonia
Simultaneous impairments of cough and swallow lead to high aspiration risk. This high risk is due to seeding of the lower airways with harmful pathogens that increase the risk of pneumonia. Mortality rates of aspiration pneumonia have been reported of over 60 percent, leading to a US$4.4 billion medical burden from hospitalized patients alone in 1997. Aspiration pneumonia costs as much as $17,000 per hospital admission. Further, this type of pneumonia can occur in as many as half of long-term care residents.
When members of our research team talk to their friends about airway protection and its consequences, everyone seems to have a story. Most center around an older relative who had a brain disorder and the difficulties this person had eating. Often their relative choked when eating or had to eat special thick foods. These are signs of impaired swallow, cough and aspiration.
Speech pathologists specialize in diagnosing and treating swallowing disorders. They often recommend thick foods that are easier to swallow and less likely to penetrate the airways during swallowing. This clinical approach is the most well-accepted.
Some companies market devices that apply a weak electrical current to the neck to improve swallowing. The long-term benefit of these devices is controversial. Further, these therapies have not been shown to enhance a weakened cough reflex.
There are no drugs for the treatment of impaired swallow or cough. It appears that the pharmaceutical industry has not yet recognized the importance of prevention of aspiration in patients with neurological disease in disease outcome.
A team in Japan has promoted a comprehensive protocol using sensory stimuli such as menthol and capsaicin, the pungent ingredient in red peppers, to help elderly people who have serious impairments in swallowing. Their preliminary results show impressive improvements in reducing aspiration pneumonias in these patients.
There is a promising approach based on strengthening breathing muscles that has been shown to improve swallow and cough function in patients with Parkinson's disease and stroke. This approach is called "expiratory muscle strength training," and it is easy for health care professionals and most patients to perform. The extent to which this method can prevent pneumonia in at-risk patients is unknown at this time.
In short, while there are some promising approaches, there are no widely accepted therapies for restoring weakened swallow and cough in patients at significant risk of aspiration. Continued research on the fundamental neurological mechanisms of coughing and swallowing will provide a foundation for new therapies to reduce the occurrence and severity of aspiration pneumonia.Provided by: The Conversation
March 17, 2017
Users of the Allen Cell Types Database can explore the morphological and electrophysiological properties of individual neurons from the mouse visual cortex. Credit: Allen Institute
The Allen Institute for Brain Science has released additional data and computer models of cell activity for inclusion in the Allen Cell Types Database: a publicly available tool for researchers to explore and understand the building blocks of the brain.
"Comprehensive coverage of hundreds to thousands of cells will be crucial for scientists who want to explore the diversity of nerve cells in the brain, and provides a base from which we can parse cells into meaningful types," says Lydia Ng, Ph.D., Senior Director of Technology at the Allen Institute for Brain Science. "This release is one more step in building a fundamental framework to help make advancements in neuroscience."
Models serve as a critical link between observed data and theories about how cells work, enabling scientists to understand the mechanisms that give rise to neuron function. Two types of models have been added and updated as part of this release. The first set are models that reduce the complexity of neurons and use cell measurements to "predict" the activity and function of those cells, which are now available for 633 neurons in the database.
Additionally, more sophisticated neuronal models based on cell shape, morphology and subcellular components are now available for hundreds of neurons via an interactive web browser.
The Allen Cell Types Database contains detailed descriptive features gathered from individual neurons in the mouse brain, including location, electrical activity and shape. For this release, electrophysiological recordings from an additional 130 cells from the cortex have been added to the database.
The Allen Cell Types Database (celltypes.brain-map.org) is a fundamental resource of the Allen Institute's ten-year plan to understand how activity in the brain leads to perception, decision-making and action. Understanding cell types—the brain's building blocks—is critical to making sense of both how the healthy brain functions and what goes wrong in diseases such as autism, Alzheimer's and Parkinson's.
Additional updates to Allen Brain Atlas resources are planned for June and October of 2017.Explore further: Allen Cell types database launched
Provided by: Allen Institute for Brain Science
Thursday, March 16, 2017
Mar. 16, 2017