Link to original article in PubMed
The results of a new study by Gigante and colleagues (2017) published in the journal Parkinsonism & Related Disorders indicates that smoking is associated with an older in age-at-onset of motor signs in patients with Parkinson's disease. These new findings are consistent with our own also showing an older age at onset of PD among ever smokers (see Ratner et al. 2014). These data provide additional support for the hypothesis that exposure to chemicals can modify the progression of PD to influence age at onset of the disease.
Link to original article in PubMed
Neurology Advisor is reporting on recent findings by Rooney and colleagues published in the journal Neurology which suggest that Hormone Replacement Therapy (HRT) provides protection against ALS. This large case control study investigated subjects from Ireland, Italy, and the Netherlands. It is important to recognize that the most common form of HRT currently in use contains conjugated equine estrogens. Animal models suggest that estradiol (E2) provides neuroprotection (Groeneveld et al., 2004). Future studies will be needed to ascertain if E2 provides greater neuroprotection than estrone (E1) in female human subjects.
Link to original story in Neurology Advisor
Link to citation in Pubmed
Dr. Dimitri Krainc, the Aaron Montgomery Ward Professor and chair of neurology at Northwestern University and Dr. Lena Burbulla, a postdoctoral fellow in his laboratory, have shown that administration of antioxidants early in the disease process may break the degenerative cycle and improve neuronal function in Parkinson's disease. These authors identified a time-dependent pathological cascade in human neurons that begins with an increase in mitochondrial oxidative stress leading to accumulation of oxidized dopamine followed by lysosomal dysfunction and α-synuclein accumulation. This neuropathological toxic cascade was not observed in mouse model PD neurons. These results are consistent with my own research suggesting that compounds that increase oxidative stress have the potential to hasten disease progression resulting in a younger age at onset of disease. Most importantly, these observations point to an opportunity to slow subclinical disease onset through early changes in lifestyle such as avoiding exposure to toxic chemicals that increase oxidative stress.
Link to Original Story in Science Daily
Link to Article in Science
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
Dr. Marcia Ratner shares and reviews the news.