Deposition of fibrillar forms of amyloid β-protein (Aβ) is commonly found in patients with Alzheimer's disease (AD) associated with cognitive decline. Impaired clearance of Aβ species is thought to be a major cause of late-onset sporadic AD. Aβ secreted into the extracellular milieu can be cleared from the brain through multiple pathways, including cellular uptake in neuronal and non-neuronal cells.
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