​Alzheimer’s Disease (AD) is a progressive brain disorder known to be the most common type of dementia in aging population, yet therapeutical curative approaches remain unmet. Epigenetics is one of the many factors that contribute to the development of the disease, and it is considered a potential therapeutical target on the search of novel pharmacological drugs. Particularly, N6-methyladenosine (m6A) RNA methylation has been shown to be one of the main dynamically reversible epigenetic modifications contributing to the progression of neural degeneration. This way, abnormal levels of m6A have been shown to be involved in the regulation of gene expression programs in various neurodegenerative diseases such as AD. Its methylation is catalyzed by the combined action of different groups of enzymes including, writers, or methylases, and erasers, or demethylases, and it is later recognized and interpreted by YTH domain family proteins known as readers. Among writers, methyltransferase-like 3 (METTL3) protein is described as a main contributor to the pathophysiology of AD.This study aimed to determine the molecular regulatory mechanism by which m6A methylation levels contribute to age-related cognitive decline. We characterized m6A levels in different AD mice models, which provided evidence of a significant decrease in disease condition, consistent with the group’s previous research on human AD brains. Particularly, our results suggest SAMP8 as a possible model organism for studying the effect of pharmacological METTL3 activation and promote future research on m6A regulatory enzymes as novel targets for the development of therapeutic drugs and treatments for AD.