Anita Ramanathan

TL;DR: It is shown that in mice overexpressing Aβ-precursor protein-overexpressing mice, pericyte loss elevates brain Aβ40 and Aβ42 levels and accelerates amyloid angiopathy and cerebral β-amyloidosis by diminishing clearance from brain interstitial fluid prior to Aβ deposition.

TL;DR: It is shown that pericyte degeneration diminishes global and individual capillary CBF responses to neuronal stimuli, resulting in neurovascular uncoupling, reduced oxygen supply to the brain and metabolic stress.

TL;DR: PICALM regulated PICALM/clathrin-dependent internalization of Aβ bound to the low density lipoprotein receptor related protein-1, a key Aβ clearance receptor, and guided Aβ trafficking to Rab5 and Rab11, leading to Aβ endothelial transcytosis and clearance.

TL;DR: It is found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons and oligodendrocytes, leading towhite-matter functional deficits before neuronal loss occurs.

TL;DR: The role of the predominant Aβ clearance protein—low-density lipoprotein receptor-related protein 1 (LRP1)—in the efflux of Aβ from the brain is discussed and the multiple factors that influence the function of LRP1-mediated A β clearance are outlined.