Alzheimer ' s Disease as a Consequence of Vascular Endothelial Dysfunction

Continued efforts to clear amyloid-β in the brain have failed produce significant benefits in Alzheimer's disease patients. This has led to a great deal of theorizing, researchers proposing other disease mechanisms, or different interpretations of the relevance of amyloid-β to the development of neurodegeneration. Most of these hypotheses will be wrong, but that doesn't prevent them from being interesting reading. One class of alternative views of Alzheimer's disease involves placing an increased emphasis on vascular dysfunction in the development of the condition, and the paper here is an example of the type.

Alzheimer's disease (AD) is the most common cause of dementia, accounting for over 70% of dementia cases in individuals above the age of 65 years. The two main pathological hallmarks of AD are extracellular deposits of the amyloid-β (Aβ) protein in the form of amyloid plaques and intracellular aggregates of hyperphosphorylated tau protein in the form of neurofibrillary tangles. Current disease models are based on the notion that abnormal protein aggregation is the primary event in AD, which begins a decade or longer prior to symptom onset, and ultimately leads to synaptic injury and neurodegeneration.

Vascular disease, including arteriolosclerosis, atherosclerosis, microinfarcts, and cerebral amyloid angiopathy (CAA), is a common co-pathology which is observed in 20-80% of AD brains at autopsy. Furthermore, almost all AD brains display evidence of en...

Source: Fight Aging! - June 8, 2023 Category: Research Authors: Reason Tags: Daily News Source Type: blogs