Kim, Baeksun Choi, Yunjung Kim, Hye-Sun Im, Heh-In 2024-01-19T19:01:36Z 2024-01-19T19:01:36Z 2021-09-04 2019-11 2093-4777 https://pubs.kist.re.kr/handle/201004/119412 Despite decades of research on Alzheimer disease, understanding the complexity of the genetic and molecular interactions involved in its pathogenesis remains far from our grasp. Methyl-CpG Binding Protein 2 (MeCP2) is an important epigenetic regulator enriched in the brain, and recent findings have implicated MeCP2 as a crucial player in Alzheimer disease. Here, we provide comprehensive insights into the pathophysiological roles of MeCP2 in Alzheimer disease. In particular, we focus on how the alteration of MeCP2 expression can impact Alzheimer disease through risk genes, amyloid-beta and tau pathology, cell death and neurodegeneration, and cellular senescence. We suggest that Alzheimer disease can be adversely affected by upregulated MeCP2-dependent repression of risk genes (MEI:2C, ADAM10, and PM20D1), increased tau accumulation, and neurodegeneration through neuronal cell death (excitotoxicity and apoptosis). In addition, we propose that the progression of Alzheimer disease could be caused by reduced MeCP2-mediated enhancement of astrocytic and microglial senescence and consequent glial SASP (senescence-associated secretory phenotype)-dependent neuroinflammation. We surmise that any imbalance in MeCP2 function would accelerate or cause Alzheimer disease pathogenesis, implying that MeCP2 may be a potential drug target for the treatment and prevention of Alzheimer disease. English KOREAN CONTINENCE SOC TRANSCRIPTION FACTOR MEF2C MESENCHYMAL STEM-CELLS RETT-SYNDROME HISTONE DEACETYLASE AMYLOID HYPOTHESIS BDNF TRANSCRIPTION DNA METHYLATION ALPHA-SECRETASE MECP2 LEVELS MOUSE MODEL Methyl-CpG Binding Protein 2 in Alzheimer Dementia Article 10.5213/inj.1938196.098 1 INTERNATIONAL NEUROUROLOGY JOURNAL, v.23, pp.S72 - S81 INTERNATIONAL NEUROUROLOGY JOURNAL 23 S72 S81 scie scopus kci ART002527006 000500297600005 2-s2.0-85076157725 Urology & Nephrology Urology & Nephrology Review TRANSCRIPTION FACTOR MEF2C MESENCHYMAL STEM-CELLS RETT-SYNDROME HISTONE DEACETYLASE AMYLOID HYPOTHESIS BDNF TRANSCRIPTION DNA METHYLATION ALPHA-SECRETASE MECP2 LEVELS MOUSE MODEL MeCP2 Alzheimer disease Risk genes Neurodegeneration Senescence Neuroinflammation