<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(6)</volume><submitter>Zuliani I</submitter><pubmed_abstract>Metformin is the first-line therapy for diabetes, even in children, and a promising attractive candidate for drug repurposing. Mitochondria are emerging as crucial targets of metformin action both in the periphery and in the brain. The present study evaluated whether treatment with metformin may rescue brain mitochondrial alterations and contrast the increased oxidative stress in a validated mouse model of Rett syndrome (RTT), a rare neurologic disorder of monogenic origin characterized by severe behavioral and physiological symptoms. No cure for RTT is available. In fully symptomatic RTT mice (12 months old MeCP2-308 heterozygous female mice), systemic treatment with metformin (100 mg/kg ip for 10 days) normalized the reduced mitochondrial ATP production and ATP levels in the whole-brain,</pubmed_abstract><journal>Journal of clinical medicine</journal><pagination>E1669</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7355965</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Anti-Diabetic Drug Metformin Rescues Aberrant Mitochondrial Activity and Restrains Oxidative Stress in a Female Mouse Model of Rett Syndrome.</pubmed_title><pmcid>PMC7355965</pmcid><pubmed_authors>Urbinati C</pubmed_authors><pubmed_authors>Cosentino L</pubmed_authors><pubmed_authors>Medici V</pubmed_authors><pubmed_authors>De Filippis B</pubmed_authors><pubmed_authors>Di Domenico F</pubmed_authors><pubmed_authors>Pietraforte D</pubmed_authors><pubmed_authors>Vacca RA</pubmed_authors><pubmed_authors>Perluigi M</pubmed_authors><pubmed_authors>Quattrini MC</pubmed_authors><pubmed_authors>Zuliani I</pubmed_authors><pubmed_authors>Valenti D</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Anti-Diabetic Drug Metformin Rescues Aberrant Mitochondrial Activity and Restrains Oxidative Stress in a Female Mouse Model of Rett Syndrome.</name><description>Metformin is the first-line therapy for diabetes, even in children, and a promising attractive candidate for drug repurposing. Mitochondria are emerging as crucial targets of metformin action both in the periphery and in the brain. The present study evaluated whether treatment with metformin may rescue brain mitochondrial alterations and contrast the increased oxidative stress in a validated mouse model of Rett syndrome (RTT), a rare neurologic disorder of monogenic origin characterized by severe behavioral and physiological symptoms. No cure for RTT is available. In fully symptomatic RTT mice (12 months old MeCP2-308 heterozygous female mice), systemic treatment with metformin (100 mg/kg ip for 10 days) normalized the reduced mitochondrial ATP production and ATP levels in the whole-brain,</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jun</publication><modification>2025-04-26T08:10:36.587Z</modification><creation>2025-04-06T12:39:19.032Z</creation></dates><accession>S-EPMC7355965</accession><cross_references><pubmed>32492904</pubmed><doi>10.3390/jcm9061669</doi></cross_references></HashMap>