<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang Y</submitter><funding>Natural Science Foundation of Hunan Provincial, China</funding><pagination>109-115</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10930482</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>47(1)</volume><pubmed_abstract>N6-methyladenosine (m6A) methylation modification is one of the most common epigenetic modifications for eukaryotic mRNA. Under the catalytic regulation of relevant enzymes, m6A participates in the body's pathophysiological processes via mediating RNA transcription, splicing, translation, and decay. In the past, we mainly focused on the regulation of m6A in tumors such as hematological tumors, cervical cancer, breast cancer. In recent years, it has been found that m6A is enriched in mRNAs of neurogenesis, cell cycle, and neuron differentiation. Its regulation in the nervous system is gradually being recognized. When the level of m6A modification and the expression levels of relevant enzyme proteins are changed, it will cause neurological dysfunction and participate in the occurrence and conversion of neurological diseases. Recent studies have found that the m6A modification and its associated enzymes were involved in major depressive disorder, Parkinson's disease, Alzheimer's disease, Fragile X syndrome, amyotrophic lateral sclerosis, and traumatic brain injury, and they also play a key role in the development of neurological diseases and many other neurological diseases. This paper mainly reviewed the recent progress of m6A modification-related enzymes, focusing on the impact of m6A modification and related enzyme-mediated regulation of gene expression on the central nervous system diseases, so as to provide potential targets for the prevention of neurological diseases.</pubmed_abstract><journal>Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences</journal><pubmed_title>Roles of m6A modification in neurological diseases.</pubmed_title><pmcid>PMC10930482</pmcid><funding_grant_id>2019JJ40257</funding_grant_id><pubmed_authors>Shi M</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Zeng J</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Li M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Roles of m6A modification in neurological diseases.</name><description>N6-methyladenosine (m6A) methylation modification is one of the most common epigenetic modifications for eukaryotic mRNA. Under the catalytic regulation of relevant enzymes, m6A participates in the body's pathophysiological processes via mediating RNA transcription, splicing, translation, and decay. In the past, we mainly focused on the regulation of m6A in tumors such as hematological tumors, cervical cancer, breast cancer. In recent years, it has been found that m6A is enriched in mRNAs of neurogenesis, cell cycle, and neuron differentiation. Its regulation in the nervous system is gradually being recognized. When the level of m6A modification and the expression levels of relevant enzyme proteins are changed, it will cause neurological dysfunction and participate in the occurrence and conversion of neurological diseases. Recent studies have found that the m6A modification and its associated enzymes were involved in major depressive disorder, Parkinson's disease, Alzheimer's disease, Fragile X syndrome, amyotrophic lateral sclerosis, and traumatic brain injury, and they also play a key role in the development of neurological diseases and many other neurological diseases. This paper mainly reviewed the recent progress of m6A modification-related enzymes, focusing on the impact of m6A modification and related enzyme-mediated regulation of gene expression on the central nervous system diseases, so as to provide potential targets for the prevention of neurological diseases.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2025-04-19T22:02:46.892Z</modification><creation>2025-04-19T22:02:46.892Z</creation></dates><accession>S-EPMC10930482</accession><cross_references><pubmed>35545370</pubmed><doi>10.11817/j.issn.1672-7347.2022.200990</doi></cross_references></HashMap>