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, April 22, 2017
April 20, 2017
Professor John Carver in his lab, holding a beaker of UHT milk. Credit: Stuart Hay, ANU
A new study on UHT milk is helping scientists to better understand Alzheimer's, Parkinson's and type 2 diabetes, opening the door to improved treatments for these age-related diseases.
Co-lead researcher, ANU Professor John Carver, said that two unrelated proteins aggregate in UHT milk over a period of months to form clusters called amyloid fibrils, which cause the milk to transform from a liquid into a gel.
He said the same type of protein clusters are found in plaque deposits in cases of Alzheimer's and Parkinson's.
"Parkinson's, dementia and type 2 diabetes are big problems for the ageing population in Australia and many other countries around the world," said Professor Carver from the ANU Research School of Chemistry.
"Our interest in milk proteins led to a discovery of the reason for this gelling phenomenon occurring in aged UHT milk."
"The research does not suggest UHT milk can cause these age-related diseases."
Professor Carver said milk proteins changed structurally when heated briefly to around 140 degrees to produce UHT milk, causing the gelling phenomenon with long-term storage.
He said normal pasteurised milk did not form amyloid fibrils.
ANU worked with CSIRO, University of Wollongong and international researchers on the study, which is published in the journal Small.
Watch a video interview with Professor John Carver about the study.
More information: Jared K. Raynes et al, Coaggregation of κ-Casein and β-Lactoglobulin Produces Morphologically Distinct Amyloid Fibrils, Small (2017). DOI: 10.1002/smll.201603591
Journal reference: Small
Provided by: Australian National University
Friday, April 21, 2017
April 16, 2017
Dysphagia (difficulty in swallowing) is a common problem in people with Parkinson's Disease. In order to assess the prevalence of dysphagia and other related symptoms, people with Parkinson's Disease presenting with dysphagia, odynophagia, heartburn, regurgitation, chest pain, and weight loss underwent evaluation using high-resolution manometry (HRM).
Most people with Parkinson's Disease (62%) experienced dysphagia (difficult swallowing), which probably contributed to weight loss in 41% of people because they were unable to eat as much. The prevalence of other symptoms was heartburn (37%), regurgitation (31%), chest pain (28%), and odynophagia (painful swallowing) (6%). Problems in the esophagus were also common.
The esophagus is through which food passes from the mouth to the stomach. The most common problems were : failure by the esophagus to contract properly (ineffective esophageal peristalsis) (55%), fragmented contraction in the esophagus (fragmented peristalsis) (48%), spasms in the esophagus (DES - diffuse esophageal spasm) (48%), and obstruction of the exit of the esophagus to the stomach (EGJ outflow obstruction) (39%). Each of these causes digestive problems.
Reference : Diseases of the Esophagus  30 (4) : 1-6 (A.Su, R.Gandhy, C.Barlow, G.Triadafilopoulos) Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/28375482
April 20, 2017
BY SARAH OWENS
Tremor, stiffness, slowness, and impaired balance—these movement-related symptoms are the hallmarks of Parkinson's disease. But they aren't the only ones. In fact, many symptoms of the disease are less visible and unrelated to movement. They include depression, anxiety, apathy, hallucinations, cognitive changes, constipation, sleeping problems, and sexual dysfunction.
Since many patients are unaware of these symptoms, they often go untreated. A new campaign by the Parkinson's Foundation—#MoreThanMotor—aims to change that by raising awareness of non-motor symptoms and encouraging patients to discuss and treat them.
Thinking Outside Motor
"In Parkinson's disease, many symptoms—loss of smell, acting out dreams, constipation, depression, and more—show up long before the onset of motor dysfunction," says Michael Okun, MD, FAAN, medical director of the Parkinson's Foundation, a merger of the National Parkinson's Foundation and the Parkinson's Disease Foundation.
As a result, he says, doctors and caregivers should be on the lookout for these symptoms, and doctors should consider Parkinson's when trying to diagnose unexplained changes in mood, loss of sex drive, sleep problems, or constipation in their patients.
#MoreThanMotor also wants to challenge the traditional view that Parkinson's "is an old person's disease," Dr. Okun says. "It's true that Parkinson's gets more common as you age, but we see the disease in teenagers and in people in their 20s, 30s, and 40s." The disease can be missed in younger patients because the symptoms are often quite different, he says. "A lot of the neuropsychiatric symptoms, such as depression and anxiety, are more common in younger patients." The disease also affects women, even though it is predominant in men, Dr. Okun adds. It's important to look out for, and treat, both motor and non-motor symptoms in all these patients.
Talk to Your Doctor
If you have Parkinson's disease and are experiencing changes in mood, such as depression and anxiety, or other, non-motor symptoms, don't wait. Talk with your doctor about ways to treat them, Dr. Okun says. Many treatments, including medications, psychotherapy, and lifestyle modifications can help.
"If you have depression, anxiety, apathy, sleeping problems, or sexual dysfunction, and you have Parkinson's disease or you think you do, talk to your doctor," Dr. Okun says. "Ask him or her what's new in treatments [for non-motor symptoms]—there have been a lot of clinical trials lately—and what the tried-and-true techniques are that can help."
Help Raise Awareness
The Parkinson's Foundation is organizing a social media "thunderclap" to promote the campaign. On April 25, all users who've signed up to participate in the thunderclap will automatically post the following message on their Facebook, Twitter, and/or Tumblr account:
#Parkinsons is #MoreThanMotor! Join me to raise awareness of the non-motor symptoms of Parkinson's: http://thndr.me/d8hJK
Join Neurology Now in participating in the thunderclap, and help raise awareness of Parkinson's non-motor symptoms, here: bit.ly/NN-PF-Thunderclap.
April 20, 2017
PET scan of a human brain with Alzheimer's disease. Credit: US National Institute on Aging, Alzheimer's Disease Education and Referral Center
A team of scientists who a few years ago identified a major pathway that leads to brain cell death in mice, have now found two drugs that block the pathway and prevent neurodegeneration. The drugs caused minimal side effects in the mice and one is already licensed for use in humans, so is ready for clinical trials.
Misfolded proteins build up in the brain in several neurodegenerative diseases and are a major factor in dementias such as Alzheimer's and Parkinson's as well as prion diseases.
Previously, the team found that the accumulation of misfolded proteins in mice with prion disease over-activates a natural defence mechanism, 'switching off' the vital production of new proteins in brain cells. They then found switching protein production back on with an experimental drug halted neurodegeneration. However, the drug tested was toxic to the pancreas and not suitable for testing in humans.
In the latest study, published today in Brain, the team tested 1,040 compounds from the National Institute for Neurological Disorders and Stroke, first in worms (C.elegans) which have a functioning nervous system and are a good experimental model for screening drugs to be used on the nervous system and then in mammalian cells. This revealed a number of suitable candidate compounds that could then be tested in mouse models of prion disease and a form of familial tauopathy (frontotemporal dementia - FTD), both of which had been protected by the experimental - but toxic - compounds in the team's previous studies.
The researchers identified two drugs that restored protein production rates in mice – trazodone hydrochloride, a licensed antidepressant, and dibenzoylmethane, a compound being trialled as an anti-cancer drug. Both drugs prevented the emergence of signs of brain cell damage in most of the prion-diseased mice and restored memory in the FTD mice. In both mouse models, the drugs reduced brain shrinkage which is a feature of neurodegenerative disease.
Professor Giovanna Mallucci, who led the team from the Medical Research Council's (MRC) Toxicology Unit in Leicester and is now based at the University of Cambridge, was today announced as one of the five associate directors of the UK Dementia Research Institute. She said: "We know that trazodone is safe to use in humans, so a clinical trial is now possible to test whether the protective effects of the drug we see on brain cells in mice with neurodegeneration also applies to people in the early stages of Alzheimer's disease and other dementias. We could know in 2-3 years whether this approach can slow down disease progression, which would be a very exciting first step in treating these disorders.
"Interestingly, trazodone has been used to treat the symptoms of patients in later stages of dementia, so we know it is safe for this group. We now need to find out whether giving the drug to patients at an early stage could help arrest or slow down the disease through its effects on this pathway."
The research was funded by the MRC and Professor Mallucci was also funded by a grant from Alzheimer's Society and Alzheimer's Drug Discovery Foundation.
Dr Rob Buckle, Chief Science Officer at the MRC, said: "This study builds on previous work by this team and is a great example of how really innovative discovery science can quite quickly translate into the possibility of real drugs to treat disease."
Dr Doug Brown, Director of Research and Development at the Alzheimer's Society, said: "We're excited by the potential of these findings. They show that a treatment approach originally discovered in mice with prion disease might also work to prevent the death of brain cells in some forms of dementia. This research is at a very early stage and has not yet been tested in people - but as one of the drugs is already available as a treatment for depression, the time taken to get from the lab to the pharmacy could be dramatically reduced."
More information: Mark Halliday et al. Repurposed drugs targeting eIF2α-P-mediated translational repression prevent neurodegeneration in mice, Brain (2017). DOI: 10.1093/brain/awx074
Journal reference: Brain
Provided by: University of Cambridge
Thursday, April 20, 2017
Wednesday, April 19, 2017
April 19, 2017
Provided by: American Academy of Neurology
New research provides evidence that an old drug may provide relief for people with advanced Parkinson's, according to a study released today that will be presented at the American Academy of Neurology's 69th Annual Meeting in Boston, April 22 to 28, 2017.
When it comes to the treatment of Parkinson's disease, the oral drug levodopa has long been considered the gold standard, improving quality of life and longevity. But as the disease progresses, the effects of the medication can partially wear off more quickly after each dose, leaving people to experience "off" time, which are periods of immobility related to temporary unresponsiveness to medication. Parkinson's symptoms, such as slowness and muscle rigidity, often make movement difficult.
"If a person with Parkinson's disease can reduce their 'off' times, that can have a great impact on their everyday life," said study author Regina Katzenschlager, MD, of Danube Hospital, affiliated with the Medical University of Vienna, Austria. "In some patients in the trial, the insecurity of unpredictable periods of incapacity was completely alleviated."
The drug apomorphine, first produced in 1865, was first used to treat advanced Parkinson's disease in the United States in 1950. Its use grew in the 1990s when European doctors starting using subcutaneous infusions of the drug to treat fluctuations in mobility that could not be controlled by the pills. Despite its use in many countries of the world, high-level evidence from randomized, blinded studies of its effectiveness and safety has up until now been lacking.
In this phase III study, researchers recruited 107 people with advanced Parkinson's disease from 23 centers in seven countries. Participants were randomly selected to receive either apomorphine subcutaneous infusion or a placebo saline infusion. The infusion was administered over a period of 14 to 18 hours each day via a small portable pump similar to the sort used in the treatment of type 1 diabetes.
The study found that those who were given apomorphine had a significantly greater reduction of "off" time than those who were given the placebo infusion, with, on average, 2.5 hours less "off" time per day, while those who received the placebo infusion had an average 30 minutes per day reduction in "off" time. This improvement was apparent within the first week of treatment. At the same time, for those who received apomorphine, there was an increase of "on" time without the abnormal involuntary movements known as dyskinesias that are often observed with levodopa.
Participants were also asked to evaluate how well they thought the treatment worked. Those who received apomorphine gave their treatment higher scores at week 12 than those who received the placebo infusion. In the apomorphine group, 71 percent of patients felt improved, compared to 18 percent on placebo, whereas 19 percent worsened on apomorphine compared to 45 percent on placebo. Apomorphine was generally well tolerated and there were no serious side effects.
"It is our hope that these findings confirming the efficacy of apomorphine infusion will encourage doctors in the United States to offer this treatment to their patients and assess its efficacy in their own clinical practice," said Katzenschlager.
Provided by: American Academy of Neurology
April 19, 2017
This is a scanning electron micrograph (false color) of a human induced pluripotent stem cell-derived neuron. Credit: Thomas Deerinck, UC San Diego
Cell biologists from Utrecht University have discovered the protein that may be the crucial traffic regulator for the transport of vital molecules inside nerve cells. When this traffic regulator is removed, the flow of traffic comes to a halt. 'Traffic jams' are reported to play a key role in neurodegenerative diseases such as Alzheimer's and Parkinson's disease. The results of their research will be published in the scientific journal Neuron on April 19.
Neurons are the main cells in the nervous system. They process information by sending, receiving, and combining signals from around the brain and the body. All neurons have a cell body where molecules vital for its functioning and maintenance are produced. The axon, a long and slender extension that can reach one metre in length in humans, sends information from the nerve cell to other nerve cells. Neuronal survival is highly dependent on the transport of vital molecules within this axon. Research has shown that defects in the transport function in the axons play a key role in degenerative brain diseases such as Alzheimer.
First comprehensive map
"Previous research examined transport processes in small areas of the axon, such as the very beginning or the very end. This left it unclear how the movement of molecules through the axon was regulated over long distances. In our study, we provide the first comprehensive map of transport in mammalian axons", says Casper Hoogenraad, Professor of Cell Biology at Utrecht University, explaining the relevance of this study.
In most neurons, an area between the cell body and the axon called the 'axon initial segment' serves as a checkpoint: only some molecules can pass through it. This area has stumped scientists for more than a decade. Why should one type of molecule be able to pass through this area, while others cannot? The answer is to be found in the traffic regulator, a protein called MAP2. "With this discovery, we have answered a fundamental question about the unique functioning of nerve cells that has occupied scientists for a long time", lead author of the study Dr Laura Gumy says.
The cell biologists from Utrecht first discovered that larger quantities of MAP2 accumulate between the cell body and the axon. When they removed MAP2 from the neuron, the normal pattern of molecule movement changed. Certain molecules suddenly ceased to enter the axon, whereas others accumulated in the axon instead of passing through to the cell body. This abnormal transport indicates that MAP2 is the driving force behind transport within the axon.
The cell biologists from Utrecht University went on to make another very important discovery. Since axons are so long, transport in the neurons is carried out by sets of proteins - known as 'motor proteins' - that carry packages of other proteins on their back. As it turns out, MAP2 is able to switch a specific 'motor protein' on or off, like a car key. This means that MAP2 actually controls which packages of molecules may enter the axon and which may not. Targeting the activity of the transport engine allowed the researchers to make another interesting discovery: MAP2 is also able to control the delivery of molecules at specific points along the axon.
New targets for therapies
"Transport within axons has been shown to fail in Alzheimer, Parkinson's disease and Huntington's disease, as well as in many other diseases. When the neuron is no longer able to control where molecules go, or is unable to get molecules to where they need to be, it cannot do its job. By understanding how transport works, we have laid the foundation for considering new targets and potential therapies for various neurodegenerative disorders", Casper Hoogenraad concludes.
More information: Neuron (2017). DOI: 10.1016/j.neuron.2017.03.046
Provided by: Utrecht University