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Conference Paper: Synaptic vesicle protein pathology in alzheimer's disease and depression

TitleSynaptic vesicle protein pathology in alzheimer's disease and depression
Authors
KeywordsMedical sciences
Psychiatry and neurology gerontology and geriatrics
Issue Date2011
PublisherElsevier Inc. The Journal's web site is located at http://www.alzheimersanddementia.org/
Citation
The 2011 The Alzheimer's Association International Conference (AAIC), Paris, France, 16-21 July 2011. In Alzheimer's & Dementia, 2011, v. 7 n. 4 suppl., p. S587, abstract no. P3-222 How to Cite?
AbstractBACKGROUND: Neuropsychiatric symptoms are common amongst Alzheimer’s disease (AD) patients. Apart from cognitive decline, AD patients often present with depression and psychosis; however, the neurobiological processes underlying these associating conditions remain unclear. Chemical synaptic transmission is crucial in the communication between neurons, and ultimately brain function. We propose synaptic dysfunction as a possible underlying mechanism for AD and depression. Furthermore, since synaptic degeneration is likely to be a relatively early pathological event, we investigated the potential neuroprotective role of antidepressants. METHODS: Primary hippocampal neurons treated with either oligomeric ß-amyloid (Aß) or corticoster one were used as an in vitro model for AD and depression, respectively. Immunocytochemical analyses of synaptic vesicle proteins were employed to investigate the pathological changes. RESULTS: Sub-lethal dosage of Aß (0.5mM) treatment for 24 hours resulted in reduction of presynaptic vesicle proteins synaptotagmin and synaptophysin. Pre-treatment for hour with antidepressants -- either imipramine or escitalopram (10mM and 20mM for both) -- were able to alleviate these pathological changes. Sub-lethal dosage of corticoster one (0.5mM) treatment for 24 hours resulted in aggregation of pre-synaptic vesicle proteins synaptotagmin and synaptophysin. Pre-treatments for hour with imipramine (10mM and 20mM) were able to alleviate these pathological changes. Pre-treatments for hour with escitalopram (10mM and 20mM) were only able to alleviate the aggregation of synaptotagmin, but not synaptophysin. CONCLUSIONS: These results show synaptic protein loss or aggregation in in vitro models of AD and depression. Antidepressants were able to alleviate some of the observed pathological changes. Further experiments will be conducted to explore the functional implications of these pathologies and the differential responses towards antidepressant treatments.
DescriptionPoster Presentations - P3
This journal supplement is the meeting abstracts of AAIC 2011
Persistent Identifierhttp://hdl.handle.net/10722/146968
ISSN
2015 Impact Factor: 11.619
2015 SCImago Journal Rankings: 4.289

 

DC FieldValueLanguage
dc.contributor.authorWuwongse, Sen_US
dc.contributor.authorHung, CHLen_US
dc.contributor.authorZhang, NQen_US
dc.contributor.authorHo, YSen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorLaw, ACKen_US
dc.date.accessioned2012-05-23T05:51:17Z-
dc.date.available2012-05-23T05:51:17Z-
dc.date.issued2011en_US
dc.identifier.citationThe 2011 The Alzheimer's Association International Conference (AAIC), Paris, France, 16-21 July 2011. In Alzheimer's & Dementia, 2011, v. 7 n. 4 suppl., p. S587, abstract no. P3-222en_US
dc.identifier.issn1552-5260-
dc.identifier.urihttp://hdl.handle.net/10722/146968-
dc.descriptionPoster Presentations - P3-
dc.descriptionThis journal supplement is the meeting abstracts of AAIC 2011-
dc.description.abstractBACKGROUND: Neuropsychiatric symptoms are common amongst Alzheimer’s disease (AD) patients. Apart from cognitive decline, AD patients often present with depression and psychosis; however, the neurobiological processes underlying these associating conditions remain unclear. Chemical synaptic transmission is crucial in the communication between neurons, and ultimately brain function. We propose synaptic dysfunction as a possible underlying mechanism for AD and depression. Furthermore, since synaptic degeneration is likely to be a relatively early pathological event, we investigated the potential neuroprotective role of antidepressants. METHODS: Primary hippocampal neurons treated with either oligomeric ß-amyloid (Aß) or corticoster one were used as an in vitro model for AD and depression, respectively. Immunocytochemical analyses of synaptic vesicle proteins were employed to investigate the pathological changes. RESULTS: Sub-lethal dosage of Aß (0.5mM) treatment for 24 hours resulted in reduction of presynaptic vesicle proteins synaptotagmin and synaptophysin. Pre-treatment for hour with antidepressants -- either imipramine or escitalopram (10mM and 20mM for both) -- were able to alleviate these pathological changes. Sub-lethal dosage of corticoster one (0.5mM) treatment for 24 hours resulted in aggregation of pre-synaptic vesicle proteins synaptotagmin and synaptophysin. Pre-treatments for hour with imipramine (10mM and 20mM) were able to alleviate these pathological changes. Pre-treatments for hour with escitalopram (10mM and 20mM) were only able to alleviate the aggregation of synaptotagmin, but not synaptophysin. CONCLUSIONS: These results show synaptic protein loss or aggregation in in vitro models of AD and depression. Antidepressants were able to alleviate some of the observed pathological changes. Further experiments will be conducted to explore the functional implications of these pathologies and the differential responses towards antidepressant treatments.-
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.alzheimersanddementia.org/-
dc.relation.ispartofAlzheimer's & Dementiaen_US
dc.subjectMedical sciences-
dc.subjectPsychiatry and neurology gerontology and geriatrics-
dc.titleSynaptic vesicle protein pathology in alzheimer's disease and depressionen_US
dc.typeConference_Paperen_US
dc.identifier.emailWuwongse, S: suthicha@hku.hken_US
dc.identifier.emailHung, CHL: chlhung@hku.hken_US
dc.identifier.emailHo, YS: janiceys@hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.emailLaw, ACK: acklaw@hku.hk-
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.doi10.1016/j.jalz.2011.05.1664-
dc.identifier.hkuros199716en_US
dc.identifier.volume7en_US
dc.identifier.issue4 suppl.en_US
dc.identifier.spageS587, abstract no. P3-222en_US
dc.identifier.epageS587, abstract no. P3-222en_US
dc.publisher.placeUnited States-
dc.description.otherThe 2011 The Alzheimer's Association International Conference (AAIC), Paris, France, 16-21 July 2011. In Alzheimer's & Dementia, 2011, v. 7 n. 4, suppl., p. S587, abstract no. P3-222-

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