{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ishii M"],"funding":["NINDS NIH HHS"],"pagination":["9096-106"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4078086"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34(27)"],"pubmed_abstract":["Weight loss is a prominent early feature of Alzheimer's disease (AD) that often precedes the cognitive decline and clinical diagnosis. While the exact pathogenesis of AD remains unclear, accumulation of amyloid-β (Aβ) derived from the amyloid precursor protein (APP) in the brain is thought to lead to the neuronal dysfunction and death underlying the dementia. In this study, we examined whether transgenic mice overexpressing the Swedish mutation of APP (Tg2576), recapitulating selected features of AD, have hypothalamic leptin signaling dysfunction leading to early body weight deficits. We found that 3-month-old Tg2576 mice, before amyloid plaque formation, exhibit decreased weight with markedly decreased adiposity, low plasma leptin levels, and increased energy expenditure without alteratio"],"journal":["The Journal of neuroscience : the official journal of the Society for Neuroscience"],"pubmed_title":["Transgenic mice overexpressing amyloid precursor protein exhibit early metabolic deficits and a pathologically low leptin state associated with hypothalamic dysfunction in arcuate neuropeptide Y neurons."],"pmcid":["PMC4078086"],"funding_grant_id":["R01 NS037853","NS37853"],"pubmed_authors":["Racchumi G","Dyke JP","Ishii M","Iadecola C","Wang G"],"additional_accession":[]},"is_claimable":false,"name":"Transgenic mice overexpressing amyloid precursor protein exhibit early metabolic deficits and a pathologically low leptin state associated with hypothalamic dysfunction in arcuate neuropeptide Y neurons.","description":"Weight loss is a prominent early feature of Alzheimer's disease (AD) that often precedes the cognitive decline and clinical diagnosis. While the exact pathogenesis of AD remains unclear, accumulation of amyloid-β (Aβ) derived from the amyloid precursor protein (APP) in the brain is thought to lead to the neuronal dysfunction and death underlying the dementia. In this study, we examined whether transgenic mice overexpressing the Swedish mutation of APP (Tg2576), recapitulating selected features of AD, have hypothalamic leptin signaling dysfunction leading to early body weight deficits. We found that 3-month-old Tg2576 mice, before amyloid plaque formation, exhibit decreased weight with markedly decreased adiposity, low plasma leptin levels, and increased energy expenditure without alteratio","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jul","modification":"2025-04-18T16:45:54.338Z","creation":"2025-04-07T04:09:34.642Z"},"accession":"S-EPMC4078086","cross_references":{"pubmed":["24990930"],"doi":["10.1523/jneurosci.0872-14.2014","10.1523/JNEUROSCI.0872-14.2014"]}}