Targeting Neuroinflammation in Alzheimer ' s Disease

As noted by the authors of today's open access review paper, Alzheimer's disease is just as strongly characterized by chronic inflammation in brain tissue as it is by the presence of aggregates of amyloid-β and phosphorylated tau. More modern views of Alzheimer's disease etiology place more emphasis on chronic inflammation as a cause of pathology, either wrapping it into the amyloid cascade hypothesis, or replacing amyloid-β with inflammatory processes in the progression of the foundational, earlier stage of the condition. The infection-senescence hypothesis, for example, suggests that persistent infection leads to cellular senescence in the supporting and immune cells of the brain (such as astrocytes and microglia), and senescent cells generate potent inflammatory signals that drive tau aggregation and the consequent widespread death of neurons. This view of senescent cells as agents of inflammation, that in turn provokes tau pathology, is supported by studies involving the use of senolytic therapies to clear senescent cells in the brains of mice engineered to produce tau aggregates. With senolytic treatment, all three metrics of senescent cell burden, chronic inflammation, and tau pathology are markedly reduced in these mouse models of tauopathy. This sort of specific theorizing and experimentation on neurodegeneration and neuroinflammation is not happening in a vacuum. There is considerable interest in a wide range of strategies that might reduce chronic in...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs