Amyloid-β-interacting proteins in peripheral fluids of Alzheimer’s disease

The accumulation of amyloid-β (Aβ) aggregates, a distinct pathological feature in Alzheimer’s disease (AD), prompts exploration into mechanisms for Aβ clearance from cerebral milieus. Notably, the efflux of Aβ 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, Aβ engages in interactions with peripheral proteins, exerting profound effects on its assembly and toxicity. This interplay extends to Aβ’s transportation to peripheral tissues and organs, responsible for its degradation and excretion. This review illustrates the intricate transfer pathways of Aβ 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.