Link to original story on Today.com
According to Glen Campbell's doctor Ronald Petersen in an interview with Today.com, saying alcohol or drug abuse caused Alzheimer’s disease is probably stretching it, "because it would mean that alcohol or drug usage actually leads to the development of plaques and tangles in the brain, and we clearly don’t know that". On the other hand, Petersen said, "severe alcohol use and certain drug behaviors can compromise the brain’s resilience. If we’ve had certain insults over our life — be it alcohol, drugs or head injuries — that may reduce the ability of the brain to compensate for the development of either aging or Alzheimer’s-type pathology. Other people who have not had those kinds insults might be able to compensate — their brains might be more plastic, more resilient — and stay functional at a higher level for a longer period."
Link to original story on Today.com
Another study reveals an association between occupational pesticide exposure and Parkinson's disease
A team of researchers from UCLA has reported on an association between occupational pesticide exposure and increased risk for PD. The study known as the Parkinson Environment Gene (PEG) study showed that risk was increased with occupational exposure to various classes of pesticides, indicating that no specific chemical but rather a shared mechanism of action may be involved. Unfortunately, this study lacked the statistical power to examine gene-pesticide interactions. Risk increased with increasing years of pesticide use, and job tasks resulting in the highest exposures to pesticides such as mixing and loading pesticides. These new findings are consistent with those reported by Ratner et al., 2015 and lend further support to the growing body of literature indicating that PD risk is modified by chemical exposures at concentrations that typically occur in occupational settings and that there is a dose response relationship between exposure and disease risk.
Link to study on PubMed
Professor Chris Exley, of Keele University is warning that survivors of the tragic Grenfell Tower fire in London were exposed to airborne aluminum which may increase their risk of Alzheimer's disease (AD) later in life. Although aluminum is toxic and was once thought to cause AD subsequent research has not supported the hypothesis that aluminum cause AD. Neuropathological findings have been reported in a patient exposed to aluminum in Camelford, Cornwall where 20 tonnes of aluminium sulphate was mistakenly discharged into the mains water supply (King et al., 2017). Bioaccumulation of aluminum in the brain has been associated with dialysis encephalopathy (Andrade et al., 2005). Increase aluminum concentration observed in brain tissue from subjects with familial Alzheimer's disease has rekindled the debate about the role this neurotoxic metal may play in this devastating neurodegenerative disease (MIzra et al., 2017).
Link to oringal story in Hippocratic Post
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.
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
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
Could a New Free Cognitive Function Screening Tool Prove Useful in the Diagnosis of Toxic Encephalopathy?
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
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
CBS News is reporting on FDA approval of the first home genetic tests for 10 health risks, including Parkinson’s disease and late-onset Alzheimer’s. “But, Dr. Jeffrey Shuren, director of the FDA’s Center for Devices, noted that "it is important that people understand that genetic risk is just one piece of the bigger puzzle. It does not mean they will or won’t ultimately develop a disease,” According to the FDA many factors contribute to lifetime risk for developing neurodegenerative disease including lifestyle and environmental factors.
Link to original story at CBSNews.com
Dr. Marcia Ratner shares and reviews the news.