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The peripheral sink hypothesis postulates that the central and peripheral pools of A\u03b2 co-exist in equilibrium. As such, cerebral amyloid levels may be modulated by intervening circulating A\u03b2. In this commentary, we discuss relevant literature supporting the potential role of peripheral A\u03b2 in exacerbating brain amyloidosis in both humans and mouse models of AD. Moreover, we highlight the need to further understand the mechanisms by which circulating A\u03b2 peptides may reach the brain and contribute to neuropathology. 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