MUST READS

An August 24, 2016 The Pharma Letter article reported that “The focus of research has shifted significantly away from established and moderately severe Alzheimer’s disease to the much earlier stages of the illness and in some cases when symptoms are very mild or even absent.”

An August 24, 2016 Time.com article highlighted the challenges that dementia poses to financial stability and to wealth managers. According to the article, “For wealth managers, the diseases present several challenges and complications. Slow progression of the illnesses may make onset difficult to ascertain; often symptoms are similar to ordinary, age-related memory loss. Clients may be in denial of the disease or hide symptoms, too. They also can fall prey to scammers, perhaps family members, raising the specter of elder financial abuse.”

RESEARCH, SCIENCE, AND TECHNOLOGY 

An August 25, 2016 News Medical article reported that “a Boston-based research team conducted a formal bias analysis and concluded that, while potentially confounding factors might have affected previous studies' results, it is doubtful that such factors totally account for observed associations between cognitive activities and a reduced risk of dementia.” According to the article: ”Our paper lends support to a potential role for late-in-life cognitive activity in prevention of Alzheimer's disease," says Deborah Blacker MD, ScD, director of the Gerontology Research Unit in the Massachusetts General Hospital Department of Psychiatry and senior author of the report in the September issue of the journal Epidemiology. "While it is possible that socioeconomic factors such as educational level might contribute to the association between cognitive activity and reduced risk, any bias introduced by such factors is probably not strong enough to fully account for the observed association.”

An August 22, 2016 Alzheimer’s News Today article reported that “Recent research has shed new light on genetic mechanisms involved in the process of neurodegenerative disease development.” According to the article, “In the recent study “UBQLN2 Mediates Autophagy-Independent Protein Aggregate Clearance by the Proteasome,” published in Cell, researchers found that when the UBQLN2 gene is undamaged and healthy in mouse models it participates in the removal of toxic proteins clumps formed in the cell which are known to cause neurodegeneration. But when the gene becomes faulty it no longer ensures this function which leads to the buildup of protein clumps and the development of neurodegeneration.”