Amyloid- β- interacting proteins in peripheral fl uids of Alzheimer's disease

Abstract

The accumulation of amyloid-beta (A beta) aggregates, a distinct pathological feature in Alzheimer's disease (AD), prompts exploration into mechanisms for A beta clearance from cerebral milieus. Notably, the efflux of A beta into peripheral fluids, encompassing the blood, cerebrospinal fluid (CSF), and lymph, emerges as a pivotal facet in its clearance. On its liberation from the cerebral realm, A beta engages in interactions with peripheral proteins, exerting profound effects on its assembly and toxicity. This interplay extends to A beta's transportation to peripheral tissues and organs, responsible for its degradation and excretion. This review illustrates the intricate transfer pathways of A beta from the brain to peripheral fluids and its interactions with peripheral proteins that can impact its aggregation and toxicity profiles associated with the pathogenesis of AD.