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postgraduate thesis: Investigation of neuroprotective effects of testosterone in primary cultured hippocampal neurons
Title | Investigation of neuroprotective effects of testosterone in primary cultured hippocampal neurons |
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Authors | |
Issue Date | 2012 |
Publisher | The University of Hong Kong (Pokfulam, Hong Kong) |
Citation | Lau, C. [劉智輝]. (2012). Investigation of neuroprotective effects of testosterone in primary cultured hippocampal neurons. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4833404 |
Abstract | Synaptic dysfunction is a critical neuropathological feature prior to the formation of extracellular senile plaques and intracellular fibrillary tangles (NFTs) in Alzheimer’s disease (AD). The synapse loss and neurites impairment lead to synaptic dysfunction that can be induced by oligomeric Aβ. The administration of oligomeric Aβ reduced the pre-synaptic vesicle proteins and altered the cytoskeletal proteins. The synaptic vesicles (SVs) playing a crucial role to transport and recycle the SV proteins and neurotransmitters (NTs) in synaptic terminals. However, the uptake and release capabilities of SVs were also disrupted by oligomeric Aβ. The disruption of SVs recycling and neurites impairment attenuate neurotransmission that exacerbates the pathogenesis of AD. Therefore, any agents can maintain the SVs recycling and protect the neurites development that could be a therapeutic target for AD.
Testosterone is a male sex steroid hormone, which is a potent therapeutic drug for neurodegenerative diseases. It has been found the neuroprotective effects for neuronal death, but the implication on synaptoprotection is still not clear. This study investigated the neuroprotective effects of testosterone from oligomeric Aβ-induced synaptic dysfunction in primary cultured hippocampal neurons. My study demonstrated that testosterone prevented Aβ-induced reduction of pre-synaptic proteins and shortening neurites. Also, testosterone could protect SVs recycling by increasing SVs unloading capability via estrogenic independent pathway. The findings reinforce the neuroprotective effects of testosterone. They are probably facilitating future development for using the concept of male sex hormone as therapy and the intervention of therapeutic drugs for AD patients. |
Degree | Master of Medical Sciences |
Subject | Testosterone - Physiological effect. Hippocampus (Brain) Neurons. |
Dept/Program | Anatomy |
Persistent Identifier | http://hdl.handle.net/10722/173849 |
HKU Library Item ID | b4833404 |
DC Field | Value | Language |
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dc.contributor.author | Lau, Chi-fai | - |
dc.contributor.author | 劉智輝 | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | Lau, C. [劉智輝]. (2012). Investigation of neuroprotective effects of testosterone in primary cultured hippocampal neurons. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4833404 | - |
dc.identifier.uri | http://hdl.handle.net/10722/173849 | - |
dc.description.abstract | Synaptic dysfunction is a critical neuropathological feature prior to the formation of extracellular senile plaques and intracellular fibrillary tangles (NFTs) in Alzheimer’s disease (AD). The synapse loss and neurites impairment lead to synaptic dysfunction that can be induced by oligomeric Aβ. The administration of oligomeric Aβ reduced the pre-synaptic vesicle proteins and altered the cytoskeletal proteins. The synaptic vesicles (SVs) playing a crucial role to transport and recycle the SV proteins and neurotransmitters (NTs) in synaptic terminals. However, the uptake and release capabilities of SVs were also disrupted by oligomeric Aβ. The disruption of SVs recycling and neurites impairment attenuate neurotransmission that exacerbates the pathogenesis of AD. Therefore, any agents can maintain the SVs recycling and protect the neurites development that could be a therapeutic target for AD. Testosterone is a male sex steroid hormone, which is a potent therapeutic drug for neurodegenerative diseases. It has been found the neuroprotective effects for neuronal death, but the implication on synaptoprotection is still not clear. This study investigated the neuroprotective effects of testosterone from oligomeric Aβ-induced synaptic dysfunction in primary cultured hippocampal neurons. My study demonstrated that testosterone prevented Aβ-induced reduction of pre-synaptic proteins and shortening neurites. Also, testosterone could protect SVs recycling by increasing SVs unloading capability via estrogenic independent pathway. The findings reinforce the neuroprotective effects of testosterone. They are probably facilitating future development for using the concept of male sex hormone as therapy and the intervention of therapeutic drugs for AD patients. | - |
dc.language | eng | - |
dc.publisher | The University of Hong Kong (Pokfulam, Hong Kong) | - |
dc.relation.ispartof | HKU Theses Online (HKUTO) | - |
dc.rights | The author retains all proprietary rights, (such as patent rights) and the right to use in future works. | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.source.uri | http://hub.hku.hk/bib/B48334042 | - |
dc.subject.lcsh | Testosterone - Physiological effect. | - |
dc.subject.lcsh | Hippocampus (Brain) | - |
dc.subject.lcsh | Neurons. | - |
dc.title | Investigation of neuroprotective effects of testosterone in primary cultured hippocampal neurons | - |
dc.type | PG_Thesis | - |
dc.identifier.hkul | b4833404 | - |
dc.description.thesisname | Master of Medical Sciences | - |
dc.description.thesislevel | Master | - |
dc.description.thesisdiscipline | Anatomy | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.5353/th_b4833404 | - |
dc.date.hkucongregation | 2012 | - |
dc.identifier.mmsid | 991033833899703414 | - |