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More Data Implicating the Role of Oxidative Stress in Parkinson's Disease

5/31/2017

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According to a new study, entitled "Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is associated with neuronal loss in Parkinson’s disease brain" by Dr. Kay Double and colleagues at the University of Sydney, Australia, the SOD1 which has been implicated in Amyotrophic Lateral Sclerosis mayday also play a role in the pathogenesis of  Parkinson’s Disease.

The story also quotes Dr. Double, who said, "We believe this loss of neurons results from a combination of oxidative stress [cell damage] and a regional deficiency in copper, both of which occur specifically in vulnerable regions of the Parkinson’s disease brain."

These data and others continue to implicate genetic and environmental factors that contribute to oxidative stress in the pathogenesis of neurodegenerative disease and emphasize the need for identifying those at risk early when efforts to reduce oxidative stress have the greatest potential to slow subclinical disease progression and forestall the emergence of debilitating clinically overt symptoms.

Link to original story by Dr. Joana Fernandes in Parkinson's News Today

Link to original per reviewed article. 
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Artificial-intelligence-proposed ALS Therapy Shows Promise in Animals

5/31/2017

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An artificial-intelligence-proposed ALS therapy delayed the onset of the disease in an animal model by promoting cellular resistance to oxidative stress. 

The project is led by Dr. Richard Mead and Dr. Laura Ferraiuolo who expect to present their findings at the Motor Neurone Disease Association 28th International Symposium in Boston in December.

These finding are consistent with those observed in epidemiological and clinical case studies which suggest that neurotoxic chemicals that increase oxidative stress can hasten subclinical disease progression and unmask latent disease.  Such therapeutics are not likely to significantly slow disease progression in the later stages but administration of such drugs to persons known to be at risk for developing ALS could delay onset sufficiently to be of clinical benefit.

Link to original article in ALS News Today
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FDA allows marketing of direct-to-consumer genetic testing  for certain conditions

5/21/2017

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The U.S. Food and Drug Administration has approved direct to consumer marketing of 23andMe Personal Genome Service Genetic Health Risk tests for 10 diseases including Parkinson's disease and late onset Alzheimer's disease.  It is important to recognize that genetic tests alone cannot determine a person’s overall risk of developing a neurodegenerative disease; this is because there are other factors that contribute to the development of a disease including environmental and occupational exposures to toxic chemicals.

Link to story on FDA News and Events Page


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Could a New Free Cognitive Function Screening Tool Prove Useful in the Diagnosis of Toxic Encephalopathy?

5/21/2017

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The THINC Task Force has developed a brief cognitive function assessment tool designed to help clinicians screen for cognitive dysfunction in their patients with depression. According to an article by Roger McIntyre in Psychiatry Advisor, this free tool which includes both subjective and objective measures of cognitive function, provides information about cognitive dysfunction expressed as a standard deviation reduction. 

Although not specifically designed to assess for cognitive deficits due to toxic encephalopathy or dementia of due to neurodegenerative disease according to John Harrison "it will likely have wider application". The application can be downloaded from the THINC-it® website. 

Link to original article in Psychiatry Advisor
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Alan Bell Busts Toxic Crime

5/19/2017

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Mercury exposure associated with increased risk for ALS

5/4/2017

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Researchers Dartmouth College presented new data at the Annual Meeting of the American Academy of Neurology suggesting that consumption of fish contaminated with mercury increases the risk for Amyotrophic Lateral Sclerosis (ALS).  Persons with higher exposure to mercury, based on toenail clippings or fish/seafood intake, had a twofold higher risk of developing ALS.  The article quoted Dr. Elijah Stommel who said "For most people, eating fish is part of a healthy diet. But questions remain about the possible impact of mercury in fish".  These new data are consistent with those from a previous study by Sienko and colleagues which showed an increased risk for ALS in patients who ate fish frequently.  Dr. Angeline S. Andrew told Medscape reporters, "these research findings suggest there may be a species- and location-dependent effect involved".  

Link to Sienko article in Archives of Neurology

Link to original article by Caroline Cassels in Medscape
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    ​Last updated: January 2, 2023.​.

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Neurotoxicants.com is strictly an information and news website about the associations between chemical exposure and neurological disease. The information provided on this site is meant to complement and not replace any advice or information from your healthcare professional. This content is not intended to be a substitute for professional medical advice or treatment.  Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.  While every care has been exercised in compiling and publishing the data contained in these pages, Neurotoxicants.com accepts no responsibility for errors or omissions to of the information provided on this website. Neurotoxicants.com cannot be held liable for typographical errors, layout error or misinformation contained herein.  Copyright © 2015-2022, Dr. Marcia H. Ratner, DABT, Proprietor and Principal Consultant, D.B.A. Neurotoxicants.com is registered with Dun and Bradstreet.  All Rights Reserved. Privately funded; Neurotoxicants.com does not accept or host paid advertising.  Neurotoxicants.com does not accept payment from any external influences which could affect the objectivity of the editorial content of this website.

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