The neuroprotective role of amyloid-β

(the discovery of upstream processes that lead to lesions will be hampered)

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Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized clinically by cognitive decline and pathologically by the accumulation of amyloid-beta-containing senile plaques and neurofibrillary tangles. A great deal of attention has focused, focused on amyloid-beta as the major pathogenic mechanism with the ultimate goal of using amyloid-beta lowering therapies as an avenue of treatment. Unfortunately, nearly a quarter century later, no tangible progress has been offered, whereas spectacular failure tends to be the most compelling. We have long contended, as has substantial literature, that proteinaceous accumulations are simply downstream and, often, endstage manifestations of disease. Their overall poor correlation with the level of dementia, and their presence in the cognitively intact is evidence that is often ignored as an inconvenient truth. Current research examining amyloid oligomers, therefore, will add copious details to what is, in essence, a reductionist distraction from upstream pleiotrophic processes such as oxidative stress, cell cycle dysfunction, and inflammation. It is now long overdue that the neuroscientists avoid the pitfall of perseverating on "proteinopathies'' and recognize that the continued targeting of end stage lesions in the face of repeated failure, or worse, is a losing proposition.
The work focuses on a synthesis of pathogenic hypotheses and their relationship with presumed causative lesions (e.g., amyloid-β) and molecules (amyloid-β, amyloid-β protein precursor). His assessment of the state of knowledge is a somewhat cynical and stinging rebuke (necessarily so in his view) of the major school of thought in Alzheimer's disease pathogenesis, which he describes as reductionist and fundamentally backward. He bases this interpretation on the pathology, and the relationship between pathology and disease that clearly indicates plaques, amyloid-β protein precursor processing, and amyloid-β metabolism, as effect, or "host response," rather than cause. Read more: ncbi.nlm.nih.gov

TODAY'S PHOTO

   

Efficacy of a medical food in mild Alzheimer's disease

Supplementation with a medical food including phosphatide precursors and cofactors for 12 weeks improved memory (delayed verbal recall) in mild AD patients. This proof-of-concept study justifies further clinical trials. Read more: sciencedirect.com

Беларусь ТВ

Posted YVN (AMYLOID @ PHOTO)