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Uptake of Amyloid beta by Glia Cells

Neuronal loss in Alzheimer’s disease (AD) is believed to result, in part, from the abnormal accumulation of Amyloid beta (A-beta) and the formation of senile plaques. Microglia and astrocytes play a central role in the elimination of A-beta. Microglia internalize soluble A-beta by pinocytosis, which can occur spontaneously or following stimulation of the P2Y4 receptor by A-beta (aa1-42). Conversely, microglia phagocytose fibrillary A-beta following activation of the complement pathway. However, the majority of oligomeric and fibrillary A-beta are cleared by microglia and astrocytes through receptor-mediated endocytosis. These glial cells express a variety of cell-surface proteins, including LRP-1, scavenger receptors, toll-like receptors, RAGE, and TREM-2, that bind A-beta and mediate its uptake.

In addition to uptake and degradation, astrocytes have been shown to play a role in the clearance of A-beta through the glymphatic system. Aquaporin 4 channels located on astrocytic endfeet that surround the CNS vasculature facilitate convective fluid transport, which drives interstitial fluid, along with extracellular solutes, into the perivascular drainage pathway. R&D Systems offers a range of research tools needed for investigating the clearance of A-beta by glial cells.