<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pharaoh G</submitter><funding>National Institute of Neurological Disorders and Stroke</funding><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institute on Aging</funding><funding>NIGMS NIH HHS</funding><pagination>1317-1331</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7060968</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>57(3)</volume><pubmed_abstract>Age-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1&lt;sup>f/f&lt;/sup> mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and g</pubmed_abstract><journal>Molecular neurobiology</journal><pubmed_title>Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function.</pubmed_title><pmcid>PMC7060968</pmcid><funding_grant_id>P20 GM103447</funding_grant_id><funding_grant_id>R01AG038747</funding_grant_id><funding_grant_id>T32AG052363</funding_grant_id><funding_grant_id>K99AG056662</funding_grant_id><funding_grant_id>R01NS056218</funding_grant_id><funding_grant_id>K99 AG056662</funding_grant_id><funding_grant_id>P30AG050911</funding_grant_id><pubmed_authors>Ashpole N</pubmed_authors><pubmed_authors>Premkumar P</pubmed_authors><pubmed_authors>Bhaskaran S</pubmed_authors><pubmed_authors>Kinter M</pubmed_authors><pubmed_authors>Pharaoh G</pubmed_authors><pubmed_authors>Van Remmen H</pubmed_authors><pubmed_authors>Logan S</pubmed_authors><pubmed_authors>Yeganeh A</pubmed_authors><pubmed_authors>Farley J</pubmed_authors><pubmed_authors>Owen D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function.</name><description>Age-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1&lt;sup>f/f&lt;/sup> mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and g</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2025-05-18T12:58:23.99Z</modification><creation>2025-05-18T12:58:23.99Z</creation></dates><accession>S-EPMC7060968</accession><cross_references><pubmed>31732912</pubmed><doi>10.1007/s12035-019-01821-4</doi></cross_references></HashMap>