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Article: Modulation of mitochondrial calcium as a pharmacological target for Alzheimer's disease

TitleModulation of mitochondrial calcium as a pharmacological target for Alzheimer's disease
Authors
Hung, CHLHo, YSChang, RCC
KeywordsAlzheimer's disease
Calcium
Mitochondria
Mitochondrial membrane potential
Voltage dependent anion channel
Issue Date2010
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/arr
Citation
Ageing Research Reviews, 2010, v. 9 n. 4, p. 447-456 How to Cite?
DOI: http://dx.doi.org/10.1016/j.arr.2010.05.003
AbstractPerturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca2+) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca2+ uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca2+ is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria. This review critically discusses the potential of manipulating mitochondrial Ca2+ concentrations as a novel therapeutic opportunity for treating AD. This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca2+ transport pathways. It is reasoned that these mitochondrial Ca2+ modulators are most effective in combination with agents that increase the Ca2+ buffering capacity of mitochondria. Modulation of mitochondrial Ca2+ handling is a potential pharmacological target for future development of AD treatments. © 2010 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/124475
ISSN
1568-1637
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.376
ISI Accession Number ID
WOS:000282866500008
Funding AgencyGrant Number
GRF755206M
761609M
NSFC/RGCN_HKU 707107M
HKU Seed Funding for Basic Science Research200911159082
HKU Alzheimer's Disease Research Network
Strategic Theme Research for Drug Discovery
Funding Information:

The work in this laboratory is supported by GRF (755206M & 761609M) and NSFC/RGC Joint Research Scheme (N_HKU 707107M), HKU Seed Funding for Basic Science Research (200911159082), HKU Alzheimer's Disease Research Network under Strategic Theme Research for Healthy Aging, and Strategic Theme Research for Drug Discovery.

References
References in Scopus
Grants
Elucidating the biological mechanisms of transforming autophagy into apoptosis in hippocampal neurons exposed to low molecular weight beta-amyloid peptide

 

DC FieldValueLanguage
dc.contributor.authorHung, CHLen_HK
dc.contributor.authorHo, YSen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2010-10-31T10:36:29Z-
dc.date.available2010-10-31T10:36:29Z-
dc.date.issued2010en_HK
dc.identifier.citationAgeing Research Reviews, 2010, v. 9 n. 4, p. 447-456en_HK
dc.identifier.issn1568-1637en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124475-
dc.description.abstractPerturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca2+) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca2+ uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca2+ is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria. This review critically discusses the potential of manipulating mitochondrial Ca2+ concentrations as a novel therapeutic opportunity for treating AD. This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca2+ transport pathways. It is reasoned that these mitochondrial Ca2+ modulators are most effective in combination with agents that increase the Ca2+ buffering capacity of mitochondria. Modulation of mitochondrial Ca2+ handling is a potential pharmacological target for future development of AD treatments. © 2010 Elsevier B.V.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/arren_HK
dc.relation.ispartofAgeing Research Reviewsen_HK
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Ageing Research Reviews. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Ageing Research Reviews, 2010, v. 9 n. 4, p. 447-456. DOI: 10.1016/j.arr.2010.05.003-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAlzheimer's diseaseen_HK
dc.subjectCalciumen_HK
dc.subjectMitochondriaen_HK
dc.subjectMitochondrial membrane potentialen_HK
dc.subjectVoltage dependent anion channelen_HK
dc.subject.meshAlzheimer Disease - metabolism - physiopathology - therapy-
dc.subject.meshCalcium - physiology-
dc.subject.meshCalcium Signaling - drug effects - physiology-
dc.subject.meshMitochondria - drug effects - physiology - ultrastructure-
dc.subject.meshMitochondrial Membranes - drug effects - physiology-
dc.titleModulation of mitochondrial calcium as a pharmacological target for Alzheimer's diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1568-1637&volume=9&issue=4&spage=447&epage=456&date=2010&atitle=Modulation+of+mitochondrial+calcium+as+a+pharmacological+target+for+Alzheimer%27s+diseaseen_HK
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.arr.2010.05.003en_HK
dc.identifier.pmid20553970-
dc.identifier.scopuseid_2-s2.0-79959236620en_HK
dc.identifier.hkuros181211en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959236620&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue4en_HK
dc.identifier.spage447en_HK
dc.identifier.epage456en_HK
dc.identifier.isiWOS:000282866500008-
dc.publisher.placeIrelanden_HK
dc.relation.projectElucidating the biological mechanisms of transforming autophagy into apoptosis in hippocampal neurons exposed to low molecular weight beta-amyloid peptide-
dc.identifier.scopusauthoridHung, CHL=54797548900en_HK
dc.identifier.scopusauthoridHo, YS=14031513600en_HK
dc.identifier.scopusauthoridChang, RCC=7403713410en_HK
dc.identifier.citeulike7244985-
dc.identifier.issnl1568-1637-

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