Epigenetic basis of Alzheimer disease

doi:10.4331/wjbc.v11.i2.62

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Sep 27, 2020 (publication date) through Jan 9, 2025

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World Journal of Biological Chemistry

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1949-8454

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Biol Chem. Sep 27, 2020; 11(2): 62-75
Published online Sep 27, 2020. doi: 10.4331/wjbc.v11.i2.62

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Figure 3 Regulation of β-amyloid production pathway and its epigenetic alterations. The deregulation of some miRNAs and some epigenetic modifications increase the production, secretion, and accumulation of β-amyloid. Furthermore, some long non-coding RNAs (lncRNA), such as lncRNA-51A, lncRNA-BC1, lncRNA-17A and lncRNA-BACE-AS are involved in the overproduction of β-amyloid. Pink and blue arrows indicate an increase and decrease of expression, respectively. AD: Alzheimer disease; APP: β-amyloid precursor protein; lncRNA: Long non-coding RNAs; miRNA: MicroRNA.

Citation: 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
URL: https://www.wjgnet.com/1949-8454/full/v11/i2/62.htm
DOI: https://dx.doi.org/10.4331/wjbc.v11.i2.62