Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.cellsig.2006.04.006
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dc.titleCellular mechanism of U18666A-mediated apoptosis in cultured murine cortical neurons: Bridging Niemann-Pick disease type C and Alzheimer's disease
dc.contributor.authorKoh, C.H.V.
dc.contributor.authorCheung, N.S.
dc.date.accessioned2011-11-29T05:58:51Z
dc.date.available2011-11-29T05:58:51Z
dc.date.issued2006
dc.identifier.citationKoh, C.H.V., Cheung, N.S. (2006). Cellular mechanism of U18666A-mediated apoptosis in cultured murine cortical neurons: Bridging Niemann-Pick disease type C and Alzheimer's disease. Cellular Signalling 18 (11) : 1844-1853. ScholarBank@NUS Repository. https://doi.org/10.1016/j.cellsig.2006.04.006
dc.identifier.issn08986568
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/28737
dc.description.abstractNeuronal cell death can occur by means of either necrosis or apoptosis. Both necrosis and apoptosis are generally believed to be distinct mechanisms of cell death with different characteristic features distinguished on the basis of their morphological and biochemical properties. The brain is the most cholesterol-rich organ in the body but not much is known about the mechanisms that regulate cholesterol homeostasis in the brain. Recently, several clinical and biochemical studies suggest that cholesterol imbalance in the brain may be a risk factor related to the development of neurological disorders such as Niemann-Pick disease type C (NPC) and Alzheimer's disease (AD). NPC is a fatal juvenile neurodegenerative disorder characterized by premature neuronal death and somatically altered cholesterol metabolism. The main biochemical manifestation in NPC is elevated intracellular accumulation of free cholesterol caused by a genetic deficit in cholesterol trafficking. The pharmacological agent, U18666A (3-β-[2-(diethylamino)ethoxy]androst-5-en-17-one), is a well-known class-2 amphiphile which inhibits cholesterol transport. Cells treated with this agent accumulate intracellular cholesterol to massive levels, similar to that observed in cells from NPC patients. NPC and AD have some pathological similarities which may share a common underlying cause. AD is one of the most common types of dementia affecting the elderly. However, the molecular mechanisms of neurodegeneration in NPC and AD are largely unknown. This review provides a consolidation of work done using U18666A in the past half century and focuses on the implications of our research findings on the mechanism of U18666A-mediated neuronal apoptosis in primary cortical neurons, which may provide an insight to elucidate the mechanisms of neurodegenerative diseases, particularly NPC and AD, where apoptosis might occur through a similar mechanism. © 2006 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.cellsig.2006.04.006
dc.sourceScopus
dc.subjectAlzheimer's disease
dc.subjectCholesterol
dc.subjectNeuronal apoptosis
dc.subjectNiemann-Pick disease type C
dc.subjectPrimary cortical neurons
dc.subjectU18666A
dc.typeReview
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1016/j.cellsig.2006.04.006
dc.description.sourcetitleCellular Signalling
dc.description.volume18
dc.description.issue11
dc.description.page1844-1853
dc.description.codenCESIE
dc.identifier.isiut000241717900003
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