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oai:repisalud.isciii.es:20.500.12105/188152024-02-27T15:23:56Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927

00925njm 22002777a 4500 dc Gamez, Nazaret author Morales, Rodrigo author 2022-09-15 While understudied, it is suspected that peripheral Aβ peptides affect Alzheimer's disease (AD)-associated pathological changes in the brain. The peripheral sink hypothesis postulates that the central and peripheral pools of Aβ co-exist in equilibrium. As such, cerebral amyloid levels may be modulated by intervening circulating Aβ. In this commentary, we discuss relevant literature supporting the potential role of peripheral Aβ 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 Aβ peptides may reach the brain and contribute to neuropathology. Finally, we discuss the implications of targeting peripheral Aβ as a therapeutic approach in treating AD. 10.1177/26331055221123072 2633-1055 Neuroscience insights http://hdl.handle.net/10668/20243 36158163 http://hdl.handle.net/20.500.12105/18815 Alzheimer’s disease amyloid-beta neurodegeneration peripheral tissues prion The Role of Circulating Aβ Seeds in the Progression of Cerebral Amyloidosis.