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Conference Paper: Investigating tau and alpha-synuclein in Parkinson’s disease dementia model

TitleInvestigating tau and alpha-synuclein in Parkinson’s disease dementia model
Authors
Issue Date2017
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NDD
Citation
Abstracts of the 13th International Conference on Alzheimer’s & Parkinson’s Diseases, Vienna, Austria, 29 March-2 April 2017. In Neurodegenerative Diseases, 2017, v. 17 n. Suppl. 1, p. 1141 How to Cite?
AbstractAims: Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease. However, the symptoms in PD stretch beyond motor impairments. About 80% of PD patients will develop Parkinson’s Disease Dementia (PDD). Cognitive functions involving executive functions, working memory and visuospatial memory are often compromised. Tau and α-synuclein have long been thought to have a central role in the development of PDD. We aim to use a classical PD model to characterize changes of tau and its relationship with α-synuclein (if any) in neurodegeneration. Method: Male Sprague Dawley rats were injected with the neurotoxin 6-hydroxydopamine (6OHDA) into the medial forebrain bundle (MFB), while controls were injected with saline. Motor dysfunction was assessed using rotarod and cylinder. Visuospatial impairment was assessed using the Morris watermaze test, while cognitive dysfunction was assessed using Y-maze and the 5-choice serial reaction time task (5-CSRTT). Tau pathology is stained for in regions connected by the MFB pathway (frontal cortex (FC), striatum (ST) and substantia nigra (SN)). Results: Our animal model fulfils PDD characteristics, with motor, cognitive and spatial deficits. Tau pathology was observed along brain regions connected by the MFB pathway. Conclusion: From the PDD model, tau pathology observed along the MFB pathway in the FC, ST, and SN is suggestive that phosphorylated-tau contributes to progressive axonal degeneration by blocking axonal transport.
DescriptionB01.a. Disease Mechanisms, Pathophysiology: Tau aggregation, phophorylation, acetylation & modifications - no. ADPD7-0687
Persistent Identifierhttp://hdl.handle.net/10722/248342
ISSN
2015 Impact Factor: 2.937
2015 SCImago Journal Rankings: 1.472

 

DC FieldValueLanguage
dc.contributor.authorPang, CCC-
dc.contributor.authorChang, RCC-
dc.date.accessioned2017-10-18T08:41:41Z-
dc.date.available2017-10-18T08:41:41Z-
dc.date.issued2017-
dc.identifier.citationAbstracts of the 13th International Conference on Alzheimer’s & Parkinson’s Diseases, Vienna, Austria, 29 March-2 April 2017. In Neurodegenerative Diseases, 2017, v. 17 n. Suppl. 1, p. 1141-
dc.identifier.issn1660-2854-
dc.identifier.urihttp://hdl.handle.net/10722/248342-
dc.descriptionB01.a. Disease Mechanisms, Pathophysiology: Tau aggregation, phophorylation, acetylation & modifications - no. ADPD7-0687-
dc.description.abstractAims: Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease. However, the symptoms in PD stretch beyond motor impairments. About 80% of PD patients will develop Parkinson’s Disease Dementia (PDD). Cognitive functions involving executive functions, working memory and visuospatial memory are often compromised. Tau and α-synuclein have long been thought to have a central role in the development of PDD. We aim to use a classical PD model to characterize changes of tau and its relationship with α-synuclein (if any) in neurodegeneration. Method: Male Sprague Dawley rats were injected with the neurotoxin 6-hydroxydopamine (6OHDA) into the medial forebrain bundle (MFB), while controls were injected with saline. Motor dysfunction was assessed using rotarod and cylinder. Visuospatial impairment was assessed using the Morris watermaze test, while cognitive dysfunction was assessed using Y-maze and the 5-choice serial reaction time task (5-CSRTT). Tau pathology is stained for in regions connected by the MFB pathway (frontal cortex (FC), striatum (ST) and substantia nigra (SN)). Results: Our animal model fulfils PDD characteristics, with motor, cognitive and spatial deficits. Tau pathology was observed along brain regions connected by the MFB pathway. Conclusion: From the PDD model, tau pathology observed along the MFB pathway in the FC, ST, and SN is suggestive that phosphorylated-tau contributes to progressive axonal degeneration by blocking axonal transport.-
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.titleInvestigating tau and alpha-synuclein in Parkinson’s disease dementia model-
dc.typeConference_Paper-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.hkuros280642-
dc.identifier.volume17-
dc.identifier.issueSuppl. 1-
dc.identifier.spage1141-
dc.identifier.epage1141-
dc.publisher.placeSwitzerland-

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