An Alzheimer ' s Hypothesis Based on Dysfunctional Synaptic Plasticity

The lack of progress towards effective therapies for Alzheimer's disease based on clearance of amyloid-β, and the relentless focus on that goal for the past two decades, has led to a great deal of alternative theorizing about the mechanisms driving the condition. Some of those theories are less well thought of than others, such as the opinion that rising use of common painkillers is the root cause of Alzheimer's. The paper here provides another example of a view of Alzheimer's disease that probably won't gain much traction in the present environment, but is nonetheless an interesting read. The sheer complexity of the aging brain still allows a great deal of room to interpret the same data in many different ways. The only real proof lies in developing a therapy that does actually produce meaningful results in humans. We can hope that first generation senolytics turn out to be that therapy, but time will tell. Numerous studies have been attempted to link Alzheimer's disease (AD)-related molecules to the pathogenesis of AD: APOE ε4-associated mechanisms such as amyloid-β (Aβ) clearance and aggregation, cerebral energy metabolism, neuroinflammation, neurovascular function, and synaptic plasticity, and presenilin-related ones such as Aβ production, calcium homeostasis, and neurogenesis. Such heterogeneous and multiple mechanistic pathways may work cumulatively over a lifetime to increase an individual's risk of AD. Nonetheless, the pathogenesis hypothesis needs to ma...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs