{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Consoli DC"],"funding":["National Institute of Environmental Health Sciences","Edward Mallinckrodt, Jr. Foundation","John F. Kennedy Center for the Performing Arts","NIDA NIH HHS","NIEHS NIH HHS","Whitehall Foundation","Brain and Behavior Research Foundation","National Institute on Drug Abuse","U.S. Department of Veterans Affairs","CSRD VA"],"pagination":["656-665"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7882008"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["157(3)"],"pubmed_abstract":["Dopamine (DA) has important roles in learning, memory, and motivational processes and is highly susceptible to oxidation. In addition to dementia, Alzheimer's disease (AD) patients frequently exhibit decreased motivation, anhedonia, and sleep disorders, suggesting deficits in dopaminergic neurotransmission. Vitamin C (ascorbate, ASC) is a critical antioxidant in the brain and is often depleted in AD patients as a result of disease-related oxidative stress and dietary deficiencies. To probe the effects of ASC deficiency and AD pathology on the DAergic system, gulo<sup>-/-</sup> mice, which like humans depend on dietary ASC to maintain adequate tissue levels, were crossed with APP/PSEN1 mice and provided sufficient or depleted ASC supplementation from weaning until 12 months of age. Ex vivo "],"journal":["Journal of neurochemistry"],"pubmed_title":["Ascorbate deficiency decreases dopamine release in gulo<sup>-/-</sup> and APP/PSEN1 mice."],"pmcid":["PMC7882008"],"funding_grant_id":["DA042111","DA048931","ES016931-12S1","R01 ES031401","CX001610","ES016931‐12S1","R01 ES016931","I01 CX001610","DP1 DA048931","R00 DA042111","ES031401-01","K99 DA042111","ES031401‐01"],"pubmed_authors":["Harrison FE","Calipari ES","Bowman AB","Consoli DC","Brady LJ"],"additional_accession":[]},"is_claimable":false,"name":"Ascorbate deficiency decreases dopamine release in gulo<sup>-/-</sup> and APP/PSEN1 mice.","description":"Dopamine (DA) has important roles in learning, memory, and motivational processes and is highly susceptible to oxidation. In addition to dementia, Alzheimer's disease (AD) patients frequently exhibit decreased motivation, anhedonia, and sleep disorders, suggesting deficits in dopaminergic neurotransmission. Vitamin C (ascorbate, ASC) is a critical antioxidant in the brain and is often depleted in AD patients as a result of disease-related oxidative stress and dietary deficiencies. To probe the effects of ASC deficiency and AD pathology on the DAergic system, gulo<sup>-/-</sup> mice, which like humans depend on dietary ASC to maintain adequate tissue levels, were crossed with APP/PSEN1 mice and provided sufficient or depleted ASC supplementation from weaning until 12 months of age. Ex vivo ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-05T10:03:16.417Z","creation":"2025-04-05T10:03:16.417Z"},"accession":"S-EPMC7882008","cross_references":{"pubmed":["32797675"],"doi":["10.1111/jnc.15151"]}}