The physiological or pharmacologically-assisted process of eliminating the abnormal, extracellular deposits of misfolded amyloid-beta peptides from the brain parenchyma. The accumulation of these insoluble plaques is a defining neuropathological feature of cognitive decline.
Origin
This clinical term is intrinsically linked to the pathology of Alzheimer’s disease, where amyloid-beta was first identified as the primary component of senile plaques. The concept of “removal” emerged from the therapeutic goal of reversing or halting the progression of protein aggregation.
Mechanism
Clearance is predominantly executed by the brain’s intrinsic immune cells, the microglia, through phagocytosis, and by the bulk flow of interstitial fluid facilitated by the glymphatic system during sleep. Optimal hormonal status, particularly estrogen and thyroid hormones, can influence microglial efficiency and the expression of necessary transport proteins. Enhancing these clearance pathways is a central strategy for neuroprotection and maintaining cognitive longevity.
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