{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jung M"],"funding":["Deutsche Forschungsgemeinschaft","Martin-Luther-Universität Halle-Wittenberg"],"pagination":["1562-1579"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10896791"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["61(3)"],"pubmed_abstract":["Late-onset Alzheimer's disease (AD) is a complex multifactorial disease. The greatest known risk factor for late-onset AD is the E4 allele of the apolipoprotein E (APOE), while increasing age is the greatest known non-genetic risk factor. The cell type-specific functions of neural stem cells (NSCs), in particular their stem cell plasticity, remain poorly explored in the context of AD pathology. Here, we describe a new model that employs late-onset AD patient-derived induced pluripotent stem cells (iPSCs) to generate NSCs and to examine the role played by APOE4 in the expression of aging markers such as sirtuin 1 (SIRT1) in comparison to healthy subjects carrying APOE3. The effect of aging was investigated by using iPSC-derived NSCs from old age subjects as healthy matched controls. Transcr"],"journal":["Molecular neurobiology"],"pubmed_title":["Neuronal Stem Cells from Late-Onset Alzheimer Patients Show Altered Regulation of Sirtuin 1 Depending on Apolipoprotein E Indicating Disturbed Stem Cell Plasticity."],"pmcid":["PMC10896791"],"funding_grant_id":["JU 3146/3-1","RTG 2155 ProMoAge"],"pubmed_authors":["Riemann D","Jung JS","Navarrete Santos A","Abid CL","Kintzel J","Pfeifer J","Puls A","Jung M","Hartmann C","Ehrhardt T","Rujescu D","Hollemann T"],"additional_accession":[]},"is_claimable":false,"name":"Neuronal Stem Cells from Late-Onset Alzheimer Patients Show Altered Regulation of Sirtuin 1 Depending on Apolipoprotein E Indicating Disturbed Stem Cell Plasticity.","description":"Late-onset Alzheimer's disease (AD) is a complex multifactorial disease. The greatest known risk factor for late-onset AD is the E4 allele of the apolipoprotein E (APOE), while increasing age is the greatest known non-genetic risk factor. The cell type-specific functions of neural stem cells (NSCs), in particular their stem cell plasticity, remain poorly explored in the context of AD pathology. Here, we describe a new model that employs late-onset AD patient-derived induced pluripotent stem cells (iPSCs) to generate NSCs and to examine the role played by APOE4 in the expression of aging markers such as sirtuin 1 (SIRT1) in comparison to healthy subjects carrying APOE3. The effect of aging was investigated by using iPSC-derived NSCs from old age subjects as healthy matched controls. Transcr","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2026-07-15T09:29:29.667Z","creation":"2024-11-07T00:57:51.698Z"},"accession":"S-EPMC10896791","cross_references":{"pubmed":["37728850"],"doi":["10.1007/s12035-023-03633-z"]}}