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Licensed 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

    Luis Fernando Hernández-ZimbrÓn is currently a postdoctoral fellow in the Oxidative Stress and Neuronal Plasticity Laboratory of the Faculty of Medicine at National Autonomous University of Mexico (UNAM) at México City, Mexico. Hernández-Zimbrón earned a Bachelor’s degree in Biology from the Faculty of Sciences at UNAM and received with honors his Doctoral degree in Biomedical Science from the Biomedical Sciences Institute at the National Autonomous University of Mexico. He is working in the field of oxidative stress in Alzheimer’s disease (AD).

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    and Selva Rivas-Arancibia

    Selva Rivas-Arancibia received her MD from the Faculty of Medicine at UNAM and received her Masters and PhD degrees in Biomedical Sciences at the same University. Currently she is Professor of Human Phisiology at the Faculty of Medicine. Dr. Rivas research interest includes ozone pollution, oxidative stress and neurodegenerative process. She is also interested in understanding the changes in the immune system caused by oxidative stress, as an inflammatory response, and the molecular mechanisms in neurodegenerative disease.


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:

About the authors

Luis Fernando Hernández-Zimbrón

Luis Fernando Hernández-ZimbrÓn is currently a postdoctoral fellow in the Oxidative Stress and Neuronal Plasticity Laboratory of the Faculty of Medicine at National Autonomous University of Mexico (UNAM) at México City, Mexico. Hernández-Zimbrón earned a Bachelor’s degree in Biology from the Faculty of Sciences at UNAM and received with honors his Doctoral degree in Biomedical Science from the Biomedical Sciences Institute at the National Autonomous University of Mexico. He is working in the field of oxidative stress in Alzheimer’s disease (AD).

Selva Rivas-Arancibia

Selva Rivas-Arancibia received her MD from the Faculty of Medicine at UNAM and received her Masters and PhD degrees in Biomedical Sciences at the same University. Currently she is Professor of Human Phisiology at the Faculty of Medicine. Dr. Rivas research interest includes ozone pollution, oxidative stress and neurodegenerative process. She is also interested in understanding the changes in the immune system caused by oxidative stress, as an inflammatory response, and the molecular mechanisms in neurodegenerative disease.


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

©2014 by De Gruyter

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