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Conference Paper: Relationship between low molecular weight beta-amyloid peptide-induced fission/fusion imbalance and mitochondrial functions

TitleRelationship between low molecular weight beta-amyloid peptide-induced fission/fusion imbalance and mitochondrial functions
Authors
KeywordsAlzheimer's disease
Beta amyloid
Mitochondria
Issue Date2010
PublisherThe Society for Neuroscience.
Citation
The 40th Annual Meeting of the Society for Neuroscience (SfN 2010), San Diego, CA., 13-17 November 2010. How to Cite?
AbstractMitochondria are involved in various vital cellular functions, ranging from bioenergetic metabolism, Ca2+ homeostasis to regulation of apoptosis. Dysfunction of mitochondria is a prominent feature in neurodegenerative diseases such as Alzheimer’s disease (AD); however the underlying mechanism of how the organelle becomes defected remains elusive. Mitochondria are dynamic organelles which continuously undergo fission and fusion to regulate their morphology and distribution. Recently, imbalance of fission/fusion has been suggested to be a novel mechanism of neurodegeneration. Nonetheless, the relationship between fission/fusion imbalance and functions of mitochondria is unclear. In the present study, we hypothesize that an imbalance of fission/fusion would result in mitochondrial dysfunction. We aim to investigate the temporal relationship between low molecular weight β-amyloid peptide (LMW Aβ)-induced impairment of mitochondrial dynamics and mitochondrial functions using different parameters. We found that LMW Aβ induced a time-dependent change in mitochondrial morphology. The length of mitochondria of hippocampal neurons treated with LMW Aβ was significantly shorter than that in control. Mitochondria changed from a long tubular network to rod-shaped and fragmented, implicating that the normal fission/fusion balance is disrupted. Different aspects of mitochondrial function were monitored at the corresponding Aβ treatment time-points using different parameters, e.g. mitochondrial superoxide production, mitochondrial Ca2+ concentration and mitochondrial membrane potential. The current study provides new insights of how mitochondrial dynamics is involved in neurodegeneration in AD.
DescriptionPoster session 247 - Alzheimer's Disease: Abeta, Energy Metabolism, Cell Signaling, Autophagy
Ref. No. 247.15/H61
Persistent Identifierhttp://hdl.handle.net/10722/142620

 

DC FieldValueLanguage
dc.contributor.authorHung, CHLen_US
dc.contributor.authorCheung, YTen_US
dc.contributor.authorWuwongse, Sen_US
dc.contributor.authorZhang, NQen_US
dc.contributor.authorChang, RCCen_US
dc.date.accessioned2011-10-28T02:53:22Z-
dc.date.available2011-10-28T02:53:22Z-
dc.date.issued2010en_US
dc.identifier.citationThe 40th Annual Meeting of the Society for Neuroscience (SfN 2010), San Diego, CA., 13-17 November 2010.en_US
dc.identifier.urihttp://hdl.handle.net/10722/142620-
dc.descriptionPoster session 247 - Alzheimer's Disease: Abeta, Energy Metabolism, Cell Signaling, Autophagy-
dc.descriptionRef. No. 247.15/H61-
dc.description.abstractMitochondria are involved in various vital cellular functions, ranging from bioenergetic metabolism, Ca2+ homeostasis to regulation of apoptosis. Dysfunction of mitochondria is a prominent feature in neurodegenerative diseases such as Alzheimer’s disease (AD); however the underlying mechanism of how the organelle becomes defected remains elusive. Mitochondria are dynamic organelles which continuously undergo fission and fusion to regulate their morphology and distribution. Recently, imbalance of fission/fusion has been suggested to be a novel mechanism of neurodegeneration. Nonetheless, the relationship between fission/fusion imbalance and functions of mitochondria is unclear. In the present study, we hypothesize that an imbalance of fission/fusion would result in mitochondrial dysfunction. We aim to investigate the temporal relationship between low molecular weight β-amyloid peptide (LMW Aβ)-induced impairment of mitochondrial dynamics and mitochondrial functions using different parameters. We found that LMW Aβ induced a time-dependent change in mitochondrial morphology. The length of mitochondria of hippocampal neurons treated with LMW Aβ was significantly shorter than that in control. Mitochondria changed from a long tubular network to rod-shaped and fragmented, implicating that the normal fission/fusion balance is disrupted. Different aspects of mitochondrial function were monitored at the corresponding Aβ treatment time-points using different parameters, e.g. mitochondrial superoxide production, mitochondrial Ca2+ concentration and mitochondrial membrane potential. The current study provides new insights of how mitochondrial dynamics is involved in neurodegeneration in AD.en_US
dc.languageengen_US
dc.publisherThe Society for Neuroscience.-
dc.relation.ispartof40th Annual Meeting of the Society for Neuroscience, SfN 2010en_US
dc.subjectAlzheimer's disease-
dc.subjectBeta amyloid-
dc.subjectMitochondria-
dc.titleRelationship between low molecular weight beta-amyloid peptide-induced fission/fusion imbalance and mitochondrial functionsen_US
dc.typeConference_Paperen_US
dc.identifier.emailHung, CHL: chlhung@hku.hken_US
dc.identifier.emailCheung, YT: esonar@gmail.com-
dc.identifier.emailWuwongse, S: suthicha@hku.hk-
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hk-
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros184446en_US
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 130715-

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