<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Philips T</submitter><funding>ALS Association</funding><funding>Department of Defense</funding><funding>NIH HHS</funding><funding>Muscular Dystrophy Association</funding><pagination>e70113</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12673003</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>74(2)</volume><pubmed_abstract>We recently reported that the loss of oligodendrocyte metabolic support through the lactate and pyruvate transporter Monocarboxylate Transporter 1 (MCT1) is well tolerated into adulthood. Only with advanced aging did we observe axonal degeneration and hypomyelination due to the loss of MCT1 from oligodendroglia lineage cells. MCT1 is also expressed by other glial subtypes, such as astrocytes and endothelial cells where it has been suggested to be essential for learning and memory tasks. However, the importance of MCT1 in these cell types for long-term axonal metabolic support is still unknown. We therefore addressed whether the conditional loss of MCT1 from either of these cell types would lead to widespread axonal degeneration with aging. Using a conditional null approach, similar to what</pubmed_abstract><journal>Glia</journal><pubmed_title>Astrocyte MCT1 Expression Does Not Contribute to the Axonal Degenerative Phenotype Observed With Ubiquitous MCT1 Depletion.</pubmed_title><pmcid>PMC12673003</pmcid><funding_grant_id>381190</funding_grant_id><pubmed_authors>Farah MH</pubmed_authors><pubmed_authors>Rothstein JD</pubmed_authors><pubmed_authors>Philips T</pubmed_authors><pubmed_authors>Spead O</pubmed_authors><pubmed_authors>Nwokeleme T</pubmed_authors><pubmed_authors>Thompson EG</pubmed_authors><pubmed_authors>Kent ER</pubmed_authors><pubmed_authors>Miller SJ</pubmed_authors><pubmed_authors>Vidensky S</pubmed_authors><pubmed_authors>Vijayakumar BG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Astrocyte MCT1 Expression Does Not Contribute to the Axonal Degenerative Phenotype Observed With Ubiquitous MCT1 Depletion.</name><description>We recently reported that the loss of oligodendrocyte metabolic support through the lactate and pyruvate transporter Monocarboxylate Transporter 1 (MCT1) is well tolerated into adulthood. Only with advanced aging did we observe axonal degeneration and hypomyelination due to the loss of MCT1 from oligodendroglia lineage cells. MCT1 is also expressed by other glial subtypes, such as astrocytes and endothelial cells where it has been suggested to be essential for learning and memory tasks. However, the importance of MCT1 in these cell types for long-term axonal metabolic support is still unknown. We therefore addressed whether the conditional loss of MCT1 from either of these cell types would lead to widespread axonal degeneration with aging. Using a conditional null approach, similar to what</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-06-06T03:10:48.755Z</modification><creation>2026-06-06T03:06:44.55Z</creation></dates><accession>S-EPMC12673003</accession><cross_references><pubmed>41331335</pubmed><doi>10.1002/glia.70113</doi></cross_references></HashMap>