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BioMed Research International
Volume 2017, Article ID 3948360, 10 pages
Review Article

Aβ Peptide Originated from Platelets Promises New Strategy in Anti-Alzheimer’s Drug Development

1School of Medicine, Department of Physiology, Universidad Central del Caribe, Bayamon, PR, USA
2School of Medicine, Department of Biochemistry, Universidad Central del Caribe, Bayamon, PR, USA

Correspondence should be addressed to Mikhail Y. Inyushin; ude.ebiraccu@nihsuyni.liahkim

Received 1 June 2017; Accepted 10 July 2017; Published 5 September 2017

Academic Editor: Xudong Huang

Copyright © 2017 Mikhail Y. Inyushin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The amyloid beta (Aβ) peptide and its deposits in the brain are known to be implicated in the neurodegeneration that occurs during Alzheimer’s disease (AD). Recently, alternative theories views concerning both the source of this peptide and its functions have been developed. It has been shown that, as in all other known types of amyloidosis, the production of Aβ originates in blood cells or cells related to blood plasma, from which it can then spread from the blood to inside the brain, with the greatest concentration around brain blood vessels. In this review, we summarize research progress in this new area and outline some future perspectives. While it is still unclear whether the main source of Aβ deposits in AD is the blood, the possibility of blocking the chain of reactions that lead to constant Aβ release from the blood to the brain may be exploited in an attempt to reduce the amyloid burden in AD. Solving the problem of Aβ accumulation in this way may provide an alternative strategy for developing anti-AD drugs.