Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/110455
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dc.titleThe roles of amyloid precursor protein (APP) in neurogenesis, implications to pathogenesis and therapy of alzheimer Disease (AD)
dc.contributor.authorZhou, Z.-D.
dc.contributor.authorChan, C.H.-S.
dc.contributor.authorMa, Q.-H.
dc.contributor.authorXu, X.-H.
dc.contributor.authorXiao, Z.-C.
dc.contributor.authorTan, E.-K.
dc.date.accessioned2014-11-26T08:32:29Z
dc.date.available2014-11-26T08:32:29Z
dc.date.issued2011-07
dc.identifier.citationZhou, Z.-D., Chan, C.H.-S., Ma, Q.-H., Xu, X.-H., Xiao, Z.-C., Tan, E.-K. (2011-07). The roles of amyloid precursor protein (APP) in neurogenesis, implications to pathogenesis and therapy of alzheimer Disease (AD). Cell Adhesion and Migration 5 (4) : -. ScholarBank@NUS Repository.
dc.identifier.issn19336918
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/110455
dc.description.abstractThe amyloid-beta (Aβ) peptide is the derivative of amyloid precursor protein (APP) generated through sequential proteolytic processing by β- and γ-secretases. Excessive accumulation of Aβ, the main constituent of amyloid plaques, has been implicated in the etiology of Alzheimer disease (AD). It was found recently that the impairments of neurogenesis in brain were associated with the pathogenesis of AD. Furthermore recent findings implicated that APP could function to influence proliferation of neural progenitor cells (NPC) and might regulate transcriptional activity of various genes. Studies demonstrated that influence of neurogenesis by APP is conferred differently via its two separate domains, soluble secreted APPs (sAPPs, mainly sAPPα) and APP intracellular domain (AICD). The sAPPα was shown to be neuroprotective and important to neurogenesis, whereas AICD was found to negatively modulate neurogenesis. Furthermore, it was demonstrated recently that microRNA could function to regulate APP expression, APP processing, Aβ accumulation and subsequently influence neurotoxicity and neurogenesis related to APP, which was implicated to AD pathogenesis, especially for sporadic AD. Based on data accumulated, secretase balances were proposed. These secretase balances could influence the downstream balance related to regulation of neurogenesis by AICD and sAPPα as well as balance related to influence of neuron viability by Aβ and sAPPα. Disruption of these secretase balances could be culprits to AD onset. © 2011 Landes Bioscience.
dc.sourceScopus
dc.subjectAlzheimer disease
dc.subjectAmyloid precursor protein
dc.subjectAmyloid-beta
dc.subjectNeural progenitor cells
dc.subjectNeurodegeneration
dc.subjectNeurogenesis
dc.typeReview
dc.contributor.departmentDUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE
dc.description.sourcetitleCell Adhesion and Migration
dc.description.volume5
dc.description.issue4
dc.description.page-
dc.identifier.isiutNOT_IN_WOS
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