{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen J"],"funding":["National Institute of Neurological Disorders and Stroke","Hong Kong Research Grants Council HKSAR","BrightFocus Foundation","NINDS NIH HHS"],"pagination":["60"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4991002"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["<h4>Background</h4>Our previous studies of Alzheimer's disease (AD) suggested that glutamine broadly improves cellular readiness to respond to stress and acts as a neuroprotectant both in vitro and in AD mouse models. We now expand our studies to a second neurodegenerative disease, ataxia-telangiectasia (A-T). Unlike AD, where clinically significant cognitive decline does not typically occur before age 65, A-T symptoms appear in early childhood and are caused exclusively by mutations in the ATM (A-T mutated) gene.<h4>Results</h4>Genetically ATM-deficient mice and wild type littermates were maintained with or without 4 % glutamine in their drinking water for several weeks. In ATM mutants, glutamine supplementation restored serum glutamine and glucose levels and reduced body weight loss. Los"],"journal":["Molecular neurodegeneration"],"pubmed_title":["The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment."],"pmcid":["PMC4991002"],"funding_grant_id":["GRF660813","R01 NS071022","1R01NS071022","AD2012101"],"pubmed_authors":["Hart RP","Li J","Chen J","Zhang Y","Chow H","Plummer MR","Chen Y","Vail G","Herrup K","Louie L"],"additional_accession":[]},"is_claimable":false,"name":"The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment.","description":"<h4>Background</h4>Our previous studies of Alzheimer's disease (AD) suggested that glutamine broadly improves cellular readiness to respond to stress and acts as a neuroprotectant both in vitro and in AD mouse models. We now expand our studies to a second neurodegenerative disease, ataxia-telangiectasia (A-T). Unlike AD, where clinically significant cognitive decline does not typically occur before age 65, A-T symptoms appear in early childhood and are caused exclusively by mutations in the ATM (A-T mutated) gene.<h4>Results</h4>Genetically ATM-deficient mice and wild type littermates were maintained with or without 4 % glutamine in their drinking water for several weeks. In ATM mutants, glutamine supplementation restored serum glutamine and glucose levels and reduced body weight loss. Los","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Aug","modification":"2025-04-26T15:55:59.032Z","creation":"2019-06-06T16:14:21Z"},"accession":"S-EPMC4991002","cross_references":{"pubmed":["27538496"],"doi":["10.1186/s13024-016-0127-y"]}}