Accessible Unlicensed Requires Authentication Published by De Gruyter July 10, 2014

Deciphering an interplay of proteins associated with amyloid β 1-42 peptide and molecular mechanisms of Alzheimer’s disease

Luis Fernando Hernández-Zimbrón and Selva Rivas-Arancibia

Abstract

Extracellular and intracellular accumulation of amyloid beta 1-42 peptide in different states of aggregation has been involved in the development and progression of Alzheimer’s disease. However, the precise mechanisms involved in amyloid beta peptide neurotoxicity have not been fully understood. There exists a wide variety of studies demonstrating the binding of amyloid beta peptide to a great variety of macromolecules and that such associations affect the cellular functions. This type of association involves proteins and receptors anchored to the plasma membrane of neurons or immune cells of the central nervous system as well as intracellular proteins that can alter intracellular transport, activate signaling pathways or affect proper mitochondrial function. In this review, we present some examples of such associations and the role played by these interactions, which are generally involved in the pathological progression of Alzheimer’s disease.


Corresponding author: Luis Fernando Hernández-Zimbrón, Faculty of Medicine, Physiology Department, National Autonomous University of Mexico, CP 04510, Mexico City, Mexico, e-mail:

Acknowledgments

Funding was provided by DGAPA-UNAM (IN221114); LFHZ is a recipient of a postdoctoral scholarship from Programa de Becas Posdoctorales, DGAPA-UNAM, México. The authors thank Varsha Velumani and Subramaniam Velumani for comments and English translation and Gevorkian G for valuable comments.

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Received: 2014-3-21
Accepted: 2014-6-1
Published Online: 2014-7-10
Published in Print: 2014-12-1

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