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Amyloid beta (Aβ) is an intricate molecule that interacts with several biomolecules and/or produces insoluble assemblies and eventually the nonphysiological depositions of its alternate with normal neuronal conditions leading to Alzheimer's disease (AD). is formed through the proteolytic cleavage of the amyloid precursor protein (APP). Significant efforts are being made to explore the exact role of in AD pathogenesis. It is believed that the deposition of in the brain takes place from components which are derived from the brain itself. However, recent evidence suggests that derived also from the periphery and hence the circulating in the blood is capable of penetrating the blood-brain barrier (BBB) and the role of derived from the periphery is largely unknown so far. Therefore, origin determination and the underlying mechanisms of its pathological effects are of considerable interest in exploring effective therapeutic strategies. The purpose of this review is to provide a novel insight into AD pathogenesis based on in both the brain and periphery and highlight new therapeutic avenues to combat AD pathogenesis. Copyright © 2020 Elsevier B.V. All rights reserved.


Md Sahab Uddin, Md Tanvir Kabir, Devesh Tewari, Abdullah Al Mamun, Bijo Mathew, Lotfi Aleya, George E Barreto, May N Bin-Jumah, Mohamed M Abdel-Daim, Ghulam Md Ashraf. Revisiting the role of brain and peripheral Aβ in the pathogenesis of Alzheimer's disease. Journal of the neurological sciences. 2020 Sep 15;416:116974

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PMID: 32559516

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