{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Swift NA"],"funding":["NIA NIH HHS","National Institutes of Health","National Institute on Aging"],"pagination":["106664"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11539201"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["201"],"pubmed_abstract":["AMP-activated protein kinase (AMPK) is an αβγ heterotrimer protein kinase that functions as a molecular sensor to maintain energy homeostasis. Accumulating evidence suggests a role of AMPK signaling in the regulation of synaptic plasticity and cognitive function; however, isoform-specific roles of AMPK in the central nervous system (CNS) remain elusive. Regulation of the AMPK activities has focused on the manipulation of the α or γ subunit. Meanwhile, accumulating evidence indicates that the β subunit is critical for sensing nutrients such as fatty acids and glycogen to control AMPK activity. Here, we generated transgenic mice with conditional suppression of either AMPKβ1 or β2 in neurons and characterized potential isoform-specific roles of AMPKβ in cognitive function and underlying mecha"],"journal":["Neurobiology of disease"],"pubmed_title":["Suppression of neuronal AMPKβ2 isoform impairs recognition memory and synaptic plasticity."],"pmcid":["PMC11539201"],"funding_grant_id":["R01 AG056622","R01 AG073823","R01 AG05581","R01 AG055581","RF1 AG082388"],"pubmed_authors":["Swift NA","Kemp BE","Yang Q","Ma T","Jester HM","Zhou X","Steinberg GR","Manuel A"],"additional_accession":[]},"is_claimable":false,"name":"Suppression of neuronal AMPKβ2 isoform impairs recognition memory and synaptic plasticity.","description":"AMP-activated protein kinase (AMPK) is an αβγ heterotrimer protein kinase that functions as a molecular sensor to maintain energy homeostasis. Accumulating evidence suggests a role of AMPK signaling in the regulation of synaptic plasticity and cognitive function; however, isoform-specific roles of AMPK in the central nervous system (CNS) remain elusive. Regulation of the AMPK activities has focused on the manipulation of the α or γ subunit. Meanwhile, accumulating evidence indicates that the β subunit is critical for sensing nutrients such as fatty acids and glycogen to control AMPK activity. Here, we generated transgenic mice with conditional suppression of either AMPKβ1 or β2 in neurons and characterized potential isoform-specific roles of AMPKβ in cognitive function and underlying mecha","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2025-04-21T22:34:40.607Z","creation":"2025-04-05T18:51:41.241Z"},"accession":"S-EPMC11539201","cross_references":{"pubmed":["39278510"],"doi":["10.1016/j.nbd.2024.106664"]}}