Not too much news from the 2017 Alzheimer's Association International Conference seemed newsworthy. You know what it is like watching an interview and you are waiting for THE question to be asked but it seems lost in all of the softballs being swung at and missed? That should be the theme. Full disclosure I am still skeptical about the entire premise of hunting for monotherapeutic cures in Alzheimer's disease. For one, they keep measuring the wrong thing. But if we are about to pivot towards prevention? Sign me up!
The Alzheimer's Association today announced the launch of a $20 million U.S. two- year clinical trial to test the ability of a multi-dimensional lifestyle intervention to prevent cognitive decline and dementia in 2,500 older adults with no current cognitive symptoms but who are at increased risk for later cognitive decline. The announcement was made at the 2017 Alzheimer's Association International Conference (AAIC 2017) in London.
The large U.S. study to PrOtect through a lifestyle INTErvention to Reduce risk (US POINTER) will include physical exercise, nutritional counseling and modification, cognitive and social stimulation, and improved self- management of medical conditions. Recruiting for the study will begin in 2018.--Press Release AAIC 2017
First, how much "protection" can we offer 60-79 year olds with co-morbid dementia risk factors "(e.g. hypertension and other cardiovascular events, elevated blood sugar)? We also forget collectively that the eponymous disease actually described early onset Alzheimer's--not what we talk about in our aging populations.
Why does it seem like diabetes and metabolic derangements are the data signature in so many chronic diseases? I would like to see this study extended to additional social determinants of health in younger at-risk populations but I remain hopeful.
Why does it seem like diabetes and metabolic derangements are the data signature in so many chronic diseases? I would like to see this study extended to additional social determinants of health in younger at-risk populations but I remain hopeful.
I don't have the answer but I do like to look at trends. Starting with a diabetes data signature and digging a little deeper seems like an interesting place to become curious.
In looking for data to see if obesity, sugar consumption, or dementia might show similar patterns--knowing correlation is not causation--but why not look where the hypothesis generation is ripe?
There is also interesting information from a brain donation program of 202 American football players. Results from the neuropathology and clinical features include evidence of cognitive decline and presence of phosphorylated tau and amyloid in addition to unique pathology associated with chronic traumatic encephalopathy. My thoughts are always perhaps the brain makes tau and amyloid in response to insults to the brain including trauma associated with head injury and the as yet not characterized trigger in Alzheimer's disease? "Deposition of amyloid-β was present in a subset of participants at all stages of CTE pathology, predominantly as diffuse amyloid-β plaques, but neuritic amyloid-β plaques and amyloid angiopathy were also present".
Click the title to download a free PDF of a report from The National Academies Press
Preventing Cognitive Decline and Dementia: A Way Forward
RCTs are the gold standard in evidence generation but require large investments of money and time. Moreover, while they are particularly effective for testing single-intervention solutions, the apparent complexity of the pathophysiology underlying cognitive decline and dementia suggests that a multifaceted approach may be most effective.