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Article: Calcium dysregulation in Alzheimer's disease: From mechanisms to therapeutic opportunities

TitleCalcium dysregulation in Alzheimer's disease: From mechanisms to therapeutic opportunities
Authors
Issue Date2009
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/pneurobio
Citation
Progress In Neurobiology, 2009, v. 89 n. 3, p. 240-255 How to Cite?
AbstractCalcium is involved in many facets of neuronal physiology, including activity, growth and differentiation, synaptic plasticity, and learning and memory, as well as pathophysiology, including necrosis, apoptosis, and degeneration. Though disturbances in calcium homeostasis in cells from Alzheimer's disease (AD) patients have been observed for many years, much more attention was focused on amyloid-β (Aβ) and tau as key causative factors for the disease. Nevertheless, increasing lines of evidence have recently reported that calcium dysregulation plays a central role in AD pathogenesis. Systemic calcium changes accompany almost the whole brain pathology process that is observed in AD, including synaptic dysfunction, mitochondrial dysfunction, presenilins mutation, Aβ production and Tau phosphorylation. Given the early and ubiquitous involvement of calcium dysregulation in AD pathogenesis, it logically presents a variety of potential therapeutic targets for AD prevention and treatment, such as calcium channels in the plasma membrane, calcium channels in the endoplasmic reticulum membrane, Aβ-formed calcium channels, calcium-related proteins. The review aims to provide an overview of the current understanding of the molecular mechanisms involved in calcium dysregulation in AD, and an insight on how to exploit calcium regulation as therapeutic opportunities in AD. © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149722
ISSN
2015 Impact Factor: 13.177
2015 SCImago Journal Rankings: 5.775
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30870884
30770757
Funding Information:

This work was supported by grants from National Natural Science Foundation of China (30870884, 30770757). We thank Dr. Robbin Henderson, Utah, USA, for critically reading this manuscript.

References

 

DC FieldValueLanguage
dc.contributor.authorYu, JTen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorTan, Len_US
dc.date.accessioned2012-06-26T05:57:37Z-
dc.date.available2012-06-26T05:57:37Z-
dc.date.issued2009en_US
dc.identifier.citationProgress In Neurobiology, 2009, v. 89 n. 3, p. 240-255en_US
dc.identifier.issn0301-0082en_US
dc.identifier.urihttp://hdl.handle.net/10722/149722-
dc.description.abstractCalcium is involved in many facets of neuronal physiology, including activity, growth and differentiation, synaptic plasticity, and learning and memory, as well as pathophysiology, including necrosis, apoptosis, and degeneration. Though disturbances in calcium homeostasis in cells from Alzheimer's disease (AD) patients have been observed for many years, much more attention was focused on amyloid-β (Aβ) and tau as key causative factors for the disease. Nevertheless, increasing lines of evidence have recently reported that calcium dysregulation plays a central role in AD pathogenesis. Systemic calcium changes accompany almost the whole brain pathology process that is observed in AD, including synaptic dysfunction, mitochondrial dysfunction, presenilins mutation, Aβ production and Tau phosphorylation. Given the early and ubiquitous involvement of calcium dysregulation in AD pathogenesis, it logically presents a variety of potential therapeutic targets for AD prevention and treatment, such as calcium channels in the plasma membrane, calcium channels in the endoplasmic reticulum membrane, Aβ-formed calcium channels, calcium-related proteins. The review aims to provide an overview of the current understanding of the molecular mechanisms involved in calcium dysregulation in AD, and an insight on how to exploit calcium regulation as therapeutic opportunities in AD. © 2009 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/pneurobioen_US
dc.relation.ispartofProgress in Neurobiologyen_US
dc.subject.meshAging - Metabolismen_US
dc.subject.meshAlzheimer Disease - Complications - Therapyen_US
dc.subject.meshAmyloid Beta-Peptides - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channels - Physiologyen_US
dc.subject.meshCalcium Signaling - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMetabolic Diseases - Etiologyen_US
dc.subject.meshMitochondrial Diseases - Metabolismen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshPresenilins - Metabolismen_US
dc.subject.meshSynapses - Physiologyen_US
dc.subject.meshTau Proteins - Metabolismen_US
dc.titleCalcium dysregulation in Alzheimer's disease: From mechanisms to therapeutic opportunitiesen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.pneurobio.2009.07.009en_US
dc.identifier.pmid19664678-
dc.identifier.scopuseid_2-s2.0-70350304571en_US
dc.identifier.hkuros170565-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350304571&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume89en_US
dc.identifier.issue3en_US
dc.identifier.spage240en_US
dc.identifier.epage255en_US
dc.identifier.isiWOS:000272369600002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYu, JT=24068133900en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridTan, L=15822952800en_US
dc.identifier.citeulike5457871-

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