Tecalco-Cruz AC, Ramírez-Jarquín JO, Alvarez-Sánchez ME, Zepeda-Cervantes J. Epigenetic basis of Alzheimer disease. World J Biol Chem 2020; 11(2): 62-75 [PMID: 33024518 DOI: 10.4331/wjbc.v11.i2.62]
Corresponding Author of This Article
Angeles C Tecalco-Cruz, PhD, Academic Research, Programa en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Av. San Lorenzo No. 290. Apdo, Mexico 03100, Mexico. angeles.tecalco@uacm.edu.mx
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Biol Chem. Sep 27, 2020; 11(2): 62-75 Published online Sep 27, 2020. doi: 10.4331/wjbc.v11.i2.62
Epigenetic basis of Alzheimer disease
Angeles C Tecalco-Cruz, Josué O Ramírez-Jarquín, María E Alvarez-Sánchez, Jesus Zepeda-Cervantes
Angeles C Tecalco-Cruz, Programa en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Mexico 03100, Mexico
Josué O Ramírez-Jarquín, División de neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico 04510, Mexico
María E Alvarez-Sánchez, Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad, Mexico 03100, Mexico
Jesus Zepeda-Cervantes, Biología celular y de desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico 04510, Mexico
Author contributions: Tecalco-Cruz AC participated in the research, organization of this article and wrote the manuscript; Ramírez-Jarquín JO, participated in the all figures of this article; Ramírez-Jarquín JO, Alvarez–Sánchez ME and Zepeda-Cervantes J participated in the research, and improvement of this article.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Angeles C Tecalco-Cruz, PhD, Academic Research, Programa en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Av. San Lorenzo No. 290. Apdo, Mexico 03100, Mexico. angeles.tecalco@uacm.edu.mx
Received: May 13, 2020 Peer-review started: May 13, 2020 First decision: June 15, 2020 Revised: June 30, 2020 Accepted: September 10, 2020 Article in press: September 10, 2020 Published online: September 27, 2020 Processing time: 134 Days and 6.9 Hours
Abstract
Alzheimer disease (AD) is the primary form of dementia that occurs spontaneously in older adults. Interestingly, the epigenetic profile of the cells forming the central nervous system changes during aging and may contribute to the progression of some neurodegenerative diseases such as AD. In this review, we present general insights into relevant epigenetic mechanisms and their relationship with aging and AD. The data suggest that some epigenetic changes during aging could be utilized as biomarkers and target molecules for the prevention and control of AD.
Core Tip: The deregulation of non-coding ribonucleic acids and epigenetic modifications have been described in Alzheimer disease (AD). These changes have been observed in different brain regions related to learning and memory, processes that are affected in AD. The epigenetic basics in the progression of AD were integrated into this review.
