Retroelements occupy 37% of the human genome and are involved in the regulation of gene expression in cis and in trans. A number of studies have shown that activation of retroelements in neuronal stem cells of the brain contributes to the genomic mosaicism required for the phenotypic diversity of differentiating neurons. These processes occur in the hippocampus, where memory is also formed, so I have proposed a hypothesis according to which retroelements are drivers of memory formation mechanisms. This is due to the sensitivity of retroelements to environmental influences and their ability to transpose into specific loci of the genome with the activation of brain-specific genes. In addition, proteins and non-coding RNAs involved in memory formation evolved from retroelements. The results of experimental articles are presented that prove this hypothesis, as well as refuting the key role of synaptic plasticity in memory consolidation. The cause of aging and neurodegenerative diseases with memory impairment is the pathological activation of retroelements, which can be influenced by specific microRNAs complementary to these retroelements. Therefore, I analyzed scientific articles in Scopus, Wos, PubMed and the MDTE DB database, which made it possible to identify 33 RE-derived microRNAs involved in Alzheimer's disease, of which 14 are associated with aging, and mechanisms of influence on the brain are described for 18 microRNAs. These microRNAs can be used as tools to target pathologically activated retroelements in aging and Alzheimer's disease to improve memory.
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