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Conference Paper: Evaluating of microtubules and tau in corticosterone-induced depression, similar pathological processes as in beta-amyloid peptide neurotoxicity

TitleEvaluating of microtubules and tau in corticosterone-induced depression, similar pathological processes as in beta-amyloid peptide neurotoxicity
Authors
KeywordsMedical sciences
Gastroenterology medical sciences
Psychiatry and neurology biology
Issue Date2015
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NDD
Citation
The 12th International Conference on Alzheimer's and Parkinson's Diseases (AD/PD™ 2015), Nice, France, 18-22 March 2015. In Neurodegenerative Diseases, 2015, v. 15 suppl. 1, p. 1786, abstract ADPD5-1707 How to Cite?
AbstractOBJECTIVES: Among different risk factors, it has been implicated that depression can be a risk factor for developing Alzheimer's disease (AD). Cytoskeleton plays important role in stabilize both axonal transport and even the spines. It has been reported for the perturbation of cytoskeleton in AD and different psychiatric disorders. Therefore, we aim to evaluate cytoskeletal protein microtubules, phosphorylation of tau and actin in experimental models of depression and AD. METHODS: We have used corticosterone as a model agent for depression and oligomeric ß-amyloid (Aß) peptide as a toxin agent for AD. We employed cultured hippocampal neurons for as our experimental model. We used live-cell imaging, Western-blot analysis and immunofluorescent staining to evaluate the stability of microtubules, phosphorylation of tau and even the abundant of postsynaptic density protein PSD-95. RESULTS: After exposure to Aß or corticosterone, aggregation of microtubules was found in neurons expressing GFP-tubulin. The level of acetylated tubulin was reduced, suggesting instable microtubules. On the other hand, increased phosphorylation of tau occurred. The effect was not limited to microtubule. By expressing mCherry-actin in cultured hippocampal neurons, Aß or corticosterone also induced actin rod formation and reduction of PSD95 protein. To maintain the stability of microtubules by taxol, all the above pathological changes could be attenuated. CONCLUSION: Our results have proved that corticosterone in depression induces similar pathological changes of microtubules and actin as if Aß in AD, which may explain why depression can be a risk factor for promoting cognitive impairment in AD.
DescriptionConference Theme: Mechanisms, Clinical Strategies, and Promising Treatments of Neurodegenerative Diseases
This FREE journal suppl. entitled: Mechanisms, Clinical Strategies, and Promising Treatments of Neurodegenerative Diseases: 12th International Conference AD/PD™, Nice, March 2015
Session: 03z. Pathophysiology & Disease Mechanisms: other
Persistent Identifierhttp://hdl.handle.net/10722/209359
ISBN
ISSN
2015 Impact Factor: 2.937
2015 SCImago Journal Rankings: 1.472

 

DC FieldValueLanguage
dc.contributor.authorChang, RCC-
dc.contributor.authorWong, GTH-
dc.contributor.authorTsang, AWT-
dc.contributor.authorHung, CHL-
dc.contributor.authorCheng, SSY-
dc.contributor.authorLaw, ACK-
dc.date.accessioned2015-04-17T05:10:07Z-
dc.date.available2015-04-17T05:10:07Z-
dc.date.issued2015-
dc.identifier.citationThe 12th International Conference on Alzheimer's and Parkinson's Diseases (AD/PD™ 2015), Nice, France, 18-22 March 2015. In Neurodegenerative Diseases, 2015, v. 15 suppl. 1, p. 1786, abstract ADPD5-1707-
dc.identifier.isbn978-3-318-05023-3-
dc.identifier.issn1660-2854-
dc.identifier.urihttp://hdl.handle.net/10722/209359-
dc.descriptionConference Theme: Mechanisms, Clinical Strategies, and Promising Treatments of Neurodegenerative Diseases-
dc.descriptionThis FREE journal suppl. entitled: Mechanisms, Clinical Strategies, and Promising Treatments of Neurodegenerative Diseases: 12th International Conference AD/PD™, Nice, March 2015-
dc.descriptionSession: 03z. Pathophysiology & Disease Mechanisms: other-
dc.description.abstractOBJECTIVES: Among different risk factors, it has been implicated that depression can be a risk factor for developing Alzheimer's disease (AD). Cytoskeleton plays important role in stabilize both axonal transport and even the spines. It has been reported for the perturbation of cytoskeleton in AD and different psychiatric disorders. Therefore, we aim to evaluate cytoskeletal protein microtubules, phosphorylation of tau and actin in experimental models of depression and AD. METHODS: We have used corticosterone as a model agent for depression and oligomeric ß-amyloid (Aß) peptide as a toxin agent for AD. We employed cultured hippocampal neurons for as our experimental model. We used live-cell imaging, Western-blot analysis and immunofluorescent staining to evaluate the stability of microtubules, phosphorylation of tau and even the abundant of postsynaptic density protein PSD-95. RESULTS: After exposure to Aß or corticosterone, aggregation of microtubules was found in neurons expressing GFP-tubulin. The level of acetylated tubulin was reduced, suggesting instable microtubules. On the other hand, increased phosphorylation of tau occurred. The effect was not limited to microtubule. By expressing mCherry-actin in cultured hippocampal neurons, Aß or corticosterone also induced actin rod formation and reduction of PSD95 protein. To maintain the stability of microtubules by taxol, all the above pathological changes could be attenuated. CONCLUSION: Our results have proved that corticosterone in depression induces similar pathological changes of microtubules and actin as if Aß in AD, which may explain why depression can be a risk factor for promoting cognitive impairment in AD.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NDD-
dc.relation.ispartofNeurodegenerative Diseases-
dc.rightsNeurodegenerative Diseases. Copyright © S Karger AG.-
dc.subjectMedical sciences-
dc.subjectGastroenterology medical sciences-
dc.subjectPsychiatry and neurology biology-
dc.titleEvaluating of microtubules and tau in corticosterone-induced depression, similar pathological processes as in beta-amyloid peptide neurotoxicity-
dc.typeConference_Paper-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.emailHung, CHL: hungchl@hku.hk-
dc.identifier.emailLaw, ACK: acklaw@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.authorityLaw, ACK=rp00262-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1159/000381736-
dc.identifier.hkuros242903-
dc.identifier.volume15-
dc.identifier.issuesuppl. 1-
dc.identifier.spage1786, abstract ADPD5-1707-
dc.identifier.epage1786, abstract ADPD5-1707-
dc.publisher.placeSwitzerland-

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