Title:Cellular Senescence and ApoE4: Their Repercussions in Alzheimer’s Disease

VOLUME: 20 ISSUE: 9

Author(s):Angeles C. Tecalco-Cruz*, Jesús Zepeda-Cervantes, Lilia López-Canovas, Josué Oriando Ramírez-Jarquín, José Pedraza-Chaverrí and Alfredo Briones-Herrera

Affiliation:Posgrado en Ciencias Genomicas, Universidad Autonoma de la Ciudad de Mexico (UACM), Apdo, Postal 03100, Ciudad de Mexico, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Apdo, Postal 04510, Ciudad de Mexico, Posgrado en Ciencias Genomicas, Universidad Autonoma de la Ciudad de Mexico (UACM), Apdo, Postal 03100, Ciudad de Mexico, Instituto de Fisiologia Celular, Universidad Nacional Autonoma de México, Apdo, Postal 04510, Ciudad de Mexico, Facultad de Quimica, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Apdo, Postal 04510, Facultad de Quimica, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Apdo, Postal 04510

Keywords:Alzheimer, ApoE, senescence, aging, neurodegeneration, AD progression.

Abstract:Alzheimer’s Disease (AD) is characterized by progressive memory loss due to neurodegeneration that occurs mainly during aging. The accumulation of senescent cells has been related to aging. Furthermore, the expression of the variant ApoE ε4 is a critical risk factor for AD. Some events that occur in senescence, such as the secretion of pro-inflammatory molecules, and metabolic and epigenetic changes, in addition to the detection of ApoE4, may accelerate the progression of AD. Here, we discuss the implications of cellular senescence and the ApoE variants in AD. Molecular studies of these risk factors for AD may hence be pivotal to define new biomarkers and novel therapeutic strategies for this neurodegenerative pathology.