2026-04-30T06:56:19Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/188152024-02-27T15:23:56Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud
author
Gamez, Nazaret
author
Morales, Rodrigo
2024-02-27T15:23:56Z
2024-02-27T15:23:56Z
2022-09-15
10.1177/26331055221123072
2633-1055
Neuroscience insights
http://hdl.handle.net/10668/20243
36158163
http://hdl.handle.net/20.500.12105/18815
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.
eng
Alzheimer’s disease
amyloid-beta
neurodegeneration
peripheral tissues
prion
The Role of Circulating Aβ Seeds in the Progression of Cerebral Amyloidosis.
research article