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ABSTRACT: Introduction
Alzheimer's disease (AD)'s multifactorial nature stresses the role of epigenetics in affecting different pathological pathways. We demonstrated that one-carbon metabolism epigenetically impacts AD-like phenotype. Here, we investigated the crosstalk between methylation and microRNAs in AD.Methods
We altered one-carbon metabolism to induce hypo- and hyper-methylation, in SK-N-BE neuroblastoma cells and TgCRND8 mice. miRNAs were profiled through a polymerase chain reaction array, then we focused on miR-29a expression and methylation of its genomic locus. Finally, we assessed miR-29a expression and methylation in the brain of AD subjects.Results
MiR-29a was repressed in hypomethylating and expressed in hypermethylating conditions. The expression of miR-29a
SUBMITTER: Raia T
PROVIDER: S-EPMC12457075 | biostudies-literature | 2025 Sep
REPOSITORIES: biostudies-literature