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Conference Paper: Characterizing the Morphological Changes and Dynamic of Mitochondria in Neurons after Exposure to ß-amyloid Peptide

TitleCharacterizing the Morphological Changes and Dynamic of Mitochondria in Neurons after Exposure to ß-amyloid Peptide
Authors
Issue Date2013
PublisherAlzheimer’s and Parkinson’s Diseases Conference.
Citation
The 11th International Conference on Alzheimer's and Parkinson's Diseases (AD/PD 2013), Florence, Italy, 6-10 March 2013 How to Cite?
AbstractObjectives: Mitochondria are the energy plant producing ATP to neurons. It has been known that mitochondria have active dynamic fission and fusion to maintain the integrity of this organelle. Many laboratories are able to measure the length of mitochondria. Many reports show the shortening of mitochondria, leading the authors to draw a conclusion of mitochondrial dysfunctions. As our laboratory focuses on how autophagy is initiated from intracellular organelle in Alzheimer's disease, we aim to re-evaluate morphology of mitochondria. Our hypothesis is that there is no significant fragmentation of mitochondria, but just morphological changes. Methods: Primary cultures of hippocampal neurons were employed in our study. We used different fluorescent protein-tagged RFP-mito, photoactivable-mito, pKillerRed-mito constructs to allow us to visualize and trace the dynamic of mitochondria in neurons under 2-photon confocal microscopy. We also used mitoSOX, Rhod-2 and TMRE to monitor the changes of oxidative stress, calcium and membrane potential of mitochondria. Results: Mitochondria displayed a change of their morphology from longitudinal to granule-shape in neurons shortly after exposure to oligomeric Aß peptide. However, there was no change of their volume, indicating no fragmentation. There was no significant reduction on membrane potential or ADP/ATP ratio. Change of their morphology was induced by oxidative stress. Conclusions: Our study reveals that mitochondria in hippocampal neurons are functional and display intact morphology. The results revise the current concept that shortening of mitochondria does not indicate any dysfunction or fragmentation of mitochondria. Our study provides indirect evidence by showing that autophagy is not initiated from mitochondria.
DescriptionConference theme: Mechanisms, clinical strategies, and promising treatments of neurodegenerative deiseases
Session Type: Basic Science
Session: Symposium 11: Mitochondria
Fulltext in: http://adpd.ekonnect.co/ADPD_443/poster_51808/program.aspx
Persistent Identifierhttp://hdl.handle.net/10722/184889

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_US
dc.contributor.authorHung, CHLen_US
dc.contributor.authorZhang, Qen_US
dc.contributor.authorHo, YSen_US
dc.date.accessioned2013-07-15T10:16:38Z-
dc.date.available2013-07-15T10:16:38Z-
dc.date.issued2013en_US
dc.identifier.citationThe 11th International Conference on Alzheimer's and Parkinson's Diseases (AD/PD 2013), Florence, Italy, 6-10 March 2013en_US
dc.identifier.urihttp://hdl.handle.net/10722/184889-
dc.descriptionConference theme: Mechanisms, clinical strategies, and promising treatments of neurodegenerative deiseases-
dc.descriptionSession Type: Basic Science-
dc.descriptionSession: Symposium 11: Mitochondria-
dc.descriptionFulltext in: http://adpd.ekonnect.co/ADPD_443/poster_51808/program.aspx-
dc.description.abstractObjectives: Mitochondria are the energy plant producing ATP to neurons. It has been known that mitochondria have active dynamic fission and fusion to maintain the integrity of this organelle. Many laboratories are able to measure the length of mitochondria. Many reports show the shortening of mitochondria, leading the authors to draw a conclusion of mitochondrial dysfunctions. As our laboratory focuses on how autophagy is initiated from intracellular organelle in Alzheimer's disease, we aim to re-evaluate morphology of mitochondria. Our hypothesis is that there is no significant fragmentation of mitochondria, but just morphological changes. Methods: Primary cultures of hippocampal neurons were employed in our study. We used different fluorescent protein-tagged RFP-mito, photoactivable-mito, pKillerRed-mito constructs to allow us to visualize and trace the dynamic of mitochondria in neurons under 2-photon confocal microscopy. We also used mitoSOX, Rhod-2 and TMRE to monitor the changes of oxidative stress, calcium and membrane potential of mitochondria. Results: Mitochondria displayed a change of their morphology from longitudinal to granule-shape in neurons shortly after exposure to oligomeric Aß peptide. However, there was no change of their volume, indicating no fragmentation. There was no significant reduction on membrane potential or ADP/ATP ratio. Change of their morphology was induced by oxidative stress. Conclusions: Our study reveals that mitochondria in hippocampal neurons are functional and display intact morphology. The results revise the current concept that shortening of mitochondria does not indicate any dysfunction or fragmentation of mitochondria. Our study provides indirect evidence by showing that autophagy is not initiated from mitochondria.-
dc.languageengen_US
dc.publisherAlzheimer’s and Parkinson’s Diseases Conference.-
dc.relation.ispartofInternational Conference on Alzheimer's and Parkinson's Diseasesen_US
dc.titleCharacterizing the Morphological Changes and Dynamic of Mitochondria in Neurons after Exposure to ß-amyloid Peptideen_US
dc.typeConference_Paperen_US
dc.identifier.emailChang, RCC: rccchang@hku.hken_US
dc.identifier.emailHung, CHL: hungchl@hku.hken_US
dc.identifier.emailHo, YS: janiceys@hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.hkuros215035en_US

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