Scientists investigating why people die from Lou Gehrig’s disease and Parkinson’s have found a new factor: high-paying or highly educated administrative jobs.
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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, July 15, 2017
PERSPECTIVES Author: Ben StecherPublished: 13 July 2017
- Ariel Hart The Atlanta Journal-Constitution
- July 13, 2017
In this photo a scientist in Florida, Matthew Disney, works on potential cures for neurodegenerative diseases like ALS. In an unrelated study, the CDC in July announced a link between certain professions and mortality from ALS and Parkinson’s disease. (Bruce Bennett/Palm Beach Post)
A study released Thursday afternoon by the U.S. Centers for Disease Control and Prevention analyzed data from several states. It found that workers in certain occupations were more likely to die from the two neurodegenerative conditions. Those occupations included computer and mathematical fields, lawyers, architects, engineers, and teachers.
Previous research has often focused on victims’ exposure to poisons at work, such as in factories, farming or the military, the study said. But this study pulled back and looked at jobs in general, and did not find a link between those professions and Parkinson’s disease or Lou Gehrig’s (also known as Amyotrophic Lateral Sclerosis, or ALS).
Other factors were already recognized, such as being older, or being male. Pesticide exposure is a factor for Parkinson’s, and cigarette smoking is a factor for ALS.
The study encouraged further investigation of the finding. For one thing, it acknowledged that they couldn’t separate what effects might come from actually having those jobs, or from simply being of a higher socioecononic status.http://www.ajc.com/news/state--regional-govt--politics/study-professions-linked-lou-gehrig-disease-and-parkinson/MbLzIswPtQYx6mN3KSQ6eK/
Friday, July 14, 2017
July 13, 2017
Glutathione is the most abundant natural antioxidant in cells. It protects them from damage and regulates a number of important functions, including cell proliferation and death, the synthesis of the genetic material and proteins and the activation of gene expression. These functions are regulated by changes in the concentration of glutathione, but the current methods do not allow for real-time measurements of glutathione levels inside cells.
Researchers at Baylor College of Medicine, Texas Children's Hospital and Rice University have moved the field of glutathione research a step forward by developing a fluorescent probe - they called it RealThiol - that can measure real-time changes of glutathione concentration in living cells. Published in Nature Communications, this study offers a new tool to investigate the roles glutathione plays in aging, health and diseases such as cancer, Alzheimer's and Parkinson's, cardiovascular conditions and diabetes, among others.
Until now, methods for measuring glutathione levels inside cells only allowed for one time point measurements," said corresponding author Dr. Jin Wang, associate professor of pharmacology and chemical biology and of molecular and cellular biology at Baylor. "We wanted to develop a method that would allow biologists to measure how glutathione concentration inside cells changes in real time."
How to measure glutathione changes in real time
Previous methods are based on irreversible chemical reactions that capture all the glutathione that is inside the cells, providing a one-time snapshot of its amount. Wang, who was trained as a physical organic chemist, and his colleagues looked for reversible chemical reactions that would capture and release glutathione, allowing for multiple measurements inside the same cell.
"Other researchers had succeeded at developing chemical probes for measuring the dynamic changes of calcium and zinc in cells using reversible chemical reactions," Wang said. "However, some researchers thought that the same could not be accomplished for glutathione."
In 2015, Wang and his colleagues published a proof of concept that a reversible reaction could be used to measure glutathione. Further research led to the current publication.
"The key contribution of the current study is that we optimized the probe and made the reaction much faster; both the forward and the reverse reaction can be completed within one minute, allowing us to follow the dynamic changes on glutathione in living cells," Wang said. "Our method requires very small amounts of the probe, which results in little toxicity and poses minimal perturbance of the antioxidant capacity in the cells, and the probe can be used in various applications, from microscopy to cell sorting experiments."
Using RealThiol, the researchers measured enhanced antioxidant capability of activated neurons and dynamic glutathione changes during ferroptosis, a form of cell death. The Wang group is currently developing glutathione probes with different sub-cellular specificities. This new tool set can potentially generate knowledge that could help develop new strategies to treat diseases involving glutathione-mediated processes.
More information: Nature Communications (2017). DOI: 10.1038/NCOMMS16087
Journal reference: Nature Communications
Provided by: Baylor College of Medicine
Thursday, July 13, 2017
NEUROSCIENCE NEWS JULY 12, 2017
Original Reserch: Abstract for “Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides” by Laibaik Park, Ken Uekawa, Lidia Garcia-Bonilla, Kenzo Koizumi, Michelle Murphy, Rose Pitstick, Linda H Younkin, Steven G Younkin, Ping Zhou, Geroge A Carlson, Josef Anrather, and Costantino Iadecola in Circulation Research. Published online May 17 doi:10.1161/CIRCRESAHA.117.311054
NEUROSCIENCE NEWS JULY 9, 2017
Two of the most common risk factors for Alzheimer’s and dementia are age and genetics. Most individuals with Alzheimer’s are 65 or older, and those who have a parent or sibling with Alzheimer’s are more likely to develop the disease. However, there is evidence to suggest that there are other factors that people can influence. NeuroscienceNews.com image is adapted from the Texas A&M news release.
By Steven Reinberg, HealthDay | July 13, 2017
Study found richer, better-educated folks with these brain diseases are more likely to die
JULY 13, 2017 BY MARTA DUARTE IN SOCIAL CLIPS.
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July 13, 2017
Researchers led by Arizona State University (ASU) and the Translational Genomics Research Institute (TGen) have identified altered expression of a gene called ANK1, which only recently has been associated with memory robbing Alzheimer's disease, in specific cells in the brain.
Using an extremely precise method of isolating cells called "laser capture microdissection," researchers looked at three specific cell types - microglia, astrocytes and neurons - in the brain tissue of individuals with a pathological diagnosis of Alzheimer's disease, and compared them to brain samples from healthy individuals and those with Parkinson's disease.
Following sequencing of each of these cell types, the ASU-TGen led team found that altered ANK1 expression originates in microglia, a type of immune cell found in the brain and central nervous system, according to the study published today in the scientific journal PLOS ONE.
"Although previous genetic and epigenetic-wide association studies had shown a significant association between ANK1 and AD, they were unable to identify the class of cells that may be responsible for such association because of the use of brain homogenates. Here, we provide evidence that microglia are the source of the previously observed differential expression patterns in the ANK1 gene in Alzheimer's disease," said Dr. Diego Mastroeni, an Assistant Research Professor at Biodesign's ASU-Banner Neurodegenerative Disease Research Center, and the study's lead author.
All three of the cell types in this study were derived from the hippocampus, a small looping structure shaped like a seahorse (its name derives from the Greek words for horse and sea monster). The hippocampus resides deep inside the human brain and plays important roles in the consolidation of both short-term and long-term memory, and in the spatial memory that enables the body to navigate.
In Alzheimer's disease - and other forms of dementia - the hippocampus is one of the first regions of the brain to suffer damage, resulting in short-term memory loss and disorientation. Individuals with extensive damage to the hippocampus are unable to form and retain new memories.
"Using our unique data set, we show that in the hippocampus, ANK1 is significantly increased four-fold in Alzheimer's disease microglia, but not in neurons or astrocytes from the same individuals," said Dr. Winnie Liang, an Assistant Professor, Director of TGen Scientific Operations and Director of TGen's Collaborative Sequencing Center, and one of the study's authors. "These findings emphasize that expression analysis of defined classes of cells is required to understand what genes and pathways are dysregulated in Alzheimer's."
Alzheimer's features many signs of chronic inflammation, and microglia are key regulators of the inflammatory cascade, proposed as an early event in the development of Alzheimer's, the study said.
Because the study found that ANK1 also was increased two-fold in Parkinson's disease, "these data suggest that alterations in ANK1, at lease in microglia, may not be disease specific, but rather a response, or phenotype associated with neurodegeneration … more specifically, neuroinflammation."
More than 5 million Americans have Alzheimer's, an irreversible and progressive brain disorder that slowly destroys memory, thinking skills and eventually the ability to conduct even the simplest of tasks. For most patients, symptoms first appear in the mid-60s. For older Americans, it is the third leading cause of death, following heart disease and cancer, according to the National Institutes of Health.
"The success of this, and many other studies, owes a great deal to the support and collaborative nature of the people of the Arizona Alzheimer's Consortium. The results obtained in this work emphasize the importance of methods that enable us to characterize the molecular profile of defined cells, either as a group or as single cells, that have been defined by any of several means," said Dr. Paul Coleman, Research Professor at Biodesign's ASU-Banner Neurodegenerative Disease Research Center, and the study's senior author.
Dr. Eric Reiman, Director of the Arizona Alzheimer's Consortium and Clinical Director of Neurogenomics at TGen, said: "This study demonstrates the value of bringing together talented researchers from different disciplines and organizations to advance the scientific fight against Alzheimer's disease."
Journal reference: PLoS ONE
Provided by: Translational Genomics Research Institute