{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Findley CA"],"funding":["NIA NIH HHS","Kenneth Stark Endowment","National Institute on Aging","Dale and Deborah Smith Center for Alzheimer’s Research and Treatment"],"pagination":["491-505"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11639043"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["102(2)"],"pubmed_abstract":["<h4>Background</h4>It is well established that glutamatergic neurotransmission plays an essential role in learning and memory. Previous studies indicate that glutamate dynamics shift with Alzheimer's disease (AD) progression, contributing to negative cognitive outcomes.<h4>Objective</h4>In this study, we characterized hippocampal glutamatergic signaling with age and disease progression in a knock-in mouse model of AD (APP<sup>NL-F/NL--F</sup>).<h4>Methods</h4>At 2-4 and 18+ months old, male and female APP<sup>NL/NL</sup>, APP<sup>NL-F/NL-F</sup>, and C57BL/6 mice underwent cognitive assessment using Morris water maze (MWM) and Novel Object Recognition (NOR). Then, basal and 70 mM KCl stimulus-evoked glutamate release was measured in the dentate gyrus (DG), CA3, and CA1 regions of the hippo"],"journal":["Journal of Alzheimer's disease : JAD"],"pubmed_title":["Sexual dimorphism, altered hippocampal glutamatergic neurotransmission, and cognitive impairment in APP knock-in mice."],"pmcid":["PMC11639043"],"funding_grant_id":["R01 AG057767","R01 AG061937","R01AG061937","R01AG057767"],"pubmed_authors":["Hill T","Peck MR","Hascup ER","McFadden SA","Quinn K","Findley CA","Hascup KN"],"additional_accession":[]},"is_claimable":false,"name":"Sexual dimorphism, altered hippocampal glutamatergic neurotransmission, and cognitive impairment in APP knock-in mice.","description":"<h4>Background</h4>It is well established that glutamatergic neurotransmission plays an essential role in learning and memory. Previous studies indicate that glutamate dynamics shift with Alzheimer's disease (AD) progression, contributing to negative cognitive outcomes.<h4>Objective</h4>In this study, we characterized hippocampal glutamatergic signaling with age and disease progression in a knock-in mouse model of AD (APP<sup>NL-F/NL--F</sup>).<h4>Methods</h4>At 2-4 and 18+ months old, male and female APP<sup>NL/NL</sup>, APP<sup>NL-F/NL-F</sup>, and C57BL/6 mice underwent cognitive assessment using Morris water maze (MWM) and Novel Object Recognition (NOR). Then, basal and 70 mM KCl stimulus-evoked glutamate release was measured in the dentate gyrus (DG), CA3, and CA1 regions of the hippo","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-05-18T03:18:53.443Z","creation":"2026-05-18T03:13:01.628Z"},"accession":"S-EPMC11639043","cross_references":{"pubmed":["39543985"],"doi":["10.3233/JAD-240795","10.3233/jad-240795"]}}