{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["45"],"submitter":["Lee IS"],"pubmed_abstract":["Alzheimer's disease (AD) is the most common cause of age-related dementia. The neuropathological hallmarks of AD include extracellular deposition of amyloid-? peptides and neurofibrillary tangles that lead to intracellular hyperphosphorylated tau in the brain. Soluble amyloid-? oligomers are the primary pathogenic factor leading to cognitive impairment in AD. Neural stem cells (NSCs) are able to self-renew and give rise to multiple neural cell lineages in both developing and adult central nervous systems. To explore the relationship between AD-related pathology and the behaviors of NSCs that enable neuroregeneration, a number of studies have used animal and in vitro models to investigate the role of amyloid-? on NSCs derived from various brain regions at different developmental stages. However, the A? effects on NSCs remain poorly understood because of conflicting results. To investigate the effects of amyloid-? oligomers on human NSCs, we established amyloid precursor protein Swedish mutant-expressing cells and identified cell-derived amyloid-? oligomers in the culture media. Human NSCs were isolated from an aborted fetal telencephalon at 13 weeks of gestation and expanded in culture as neurospheres. Human NSCs exposure to cell-derived amyloid-? oligomers decreased dividing potential resulting from senescence through telomere attrition, impaired neurogenesis and promoted gliogenesis, and attenuated mobility. These amyloid-? oligomers modulated the proliferation, differentiation and migration patterns of human NSCs via a glycogen synthase kinase-3?-mediated signaling pathway. These findings contribute to the development of human NSC-based therapy for AD by elucidating the effects of A? oligomers on human NSCs."],"journal":["Experimental & molecular medicine"],"pagination":["e60"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3849574"],"repository":["biostudies-literature"],"pubmed_title":["Amyloid-? oligomers regulate the properties of human neural stem cells through GSK-3? signaling."],"pmcid":["PMC3849574"],"pubmed_authors":["Lee IS","Park KI","Jung K","Kim IS"],"additional_accession":[]},"is_claimable":false,"name":"Amyloid-? oligomers regulate the properties of human neural stem cells through GSK-3? signaling.","description":"Alzheimer's disease (AD) is the most common cause of age-related dementia. The neuropathological hallmarks of AD include extracellular deposition of amyloid-? peptides and neurofibrillary tangles that lead to intracellular hyperphosphorylated tau in the brain. Soluble amyloid-? oligomers are the primary pathogenic factor leading to cognitive impairment in AD. Neural stem cells (NSCs) are able to self-renew and give rise to multiple neural cell lineages in both developing and adult central nervous systems. To explore the relationship between AD-related pathology and the behaviors of NSCs that enable neuroregeneration, a number of studies have used animal and in vitro models to investigate the role of amyloid-? on NSCs derived from various brain regions at different developmental stages. However, the A? effects on NSCs remain poorly understood because of conflicting results. To investigate the effects of amyloid-? oligomers on human NSCs, we established amyloid precursor protein Swedish mutant-expressing cells and identified cell-derived amyloid-? oligomers in the culture media. Human NSCs were isolated from an aborted fetal telencephalon at 13 weeks of gestation and expanded in culture as neurospheres. Human NSCs exposure to cell-derived amyloid-? oligomers decreased dividing potential resulting from senescence through telomere attrition, impaired neurogenesis and promoted gliogenesis, and attenuated mobility. These amyloid-? oligomers modulated the proliferation, differentiation and migration patterns of human NSCs via a glycogen synthase kinase-3?-mediated signaling pathway. These findings contribute to the development of human NSC-based therapy for AD by elucidating the effects of A? oligomers on human NSCs.","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Nov","modification":"2021-02-25T08:17:30Z","creation":"2019-03-27T03:09:43Z"},"accession":"S-EPMC3849574","cross_references":{"pubmed":["24232259"],"doi":["10.1038/emm.2013.125"]}}