As a companion piece to recent research on immune dysfunction in the central nervous system as the bridge between early amyloid-β and later tau pathology in Alzheimer’s disease, here is a another recent discussion of work demonstrating cellular senescence to arise from amyloid-β aggregation in the brain. In this view of Alzheimer’s disease, the primary reason why amyloid-β plaques set the stage for the later, much more harmful phase of the condition, is that the plaques cause cells to become senescent. These cells secrete a mix of inflammatory signals, and the consequent neuroinflammation and dysfunction of immune cells spurs aggregation of tau into neurofibrillary tangles. That in turn causes cell death, synaptic destruction, dementia, and death.
Fortunately, these new discoveries strongly suggest that senolytic therapies that can bypass the blood-brain barrier should be effective in treating Alzheimer’s disease. Quite effective in comparison to any existing therapy, at least, which is admittedly a low bar to pass at this point in time. Nonetheless, given the robust results produced by senolytics for all of the other most common inflammatory conditions of aging in animal studies, we might be optimistic. Recent demonstrations in
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