2022 神醫中心學術演講 9 (現場+視訊)
日期 : 10月 25日星期二
時間 : 上午11:00
地點 : 國衛院竹南院區/ 行政大樓B1第6會議室
主題 : Anti-alpha-synuclein immunotherapy for Parkinson’s disease
講師 : 陳雲翔 輔仁大學理工學院生命科學系／本中心合聘副研究員
報名連結
| 視訊系統 Webex : 會議連結 密碼: 1234 |
摘要
Accumulation of α-synuclein (αSyn) in the dopaminergic neurons is a common pathology
in patients with Parkinson’s disease (PD). Overproduction of αSyn promotes the formation
of oligomeric αSyn aggregates and enhances the degeneration of dopaminergic neurons.
Therefore, downregulating αSyn protein levels to prevent or decrease αSyn aggregation is
a potential therapeutic strategy to attenuate the progression of PD. I would like to share
our experience in the investigation of anti-αSyn immunotherapy for PD and look forward to
receiving your suggestion. We recently identified a single-chain intrabody (NAC32)
capable of reducing αSyn protein levels in mammalian cell lines and the rat brain. This
intrabody was further shown to attenuate αSyn-mediated motor deficits and degeneration
of dopaminergic neurons in rats selectively overexpressing αSyn in the substantia nigra.
Similar protection effects were also found in aging rats receiving nigra injection of adenoassociated viruses (AAV) encoding NAC32 intrabody. In addition, AAV-mediated peripheral
expression of a single-chain antibody targeting the C-terminal of αSyn improved motor
activity in mice transduced with AAV encoding αSyn in the substantia nigra. Collectively,
passive immunization against αSyn could be a potential treatment for synucleinopathy or
PD, although further investigation is required. On the other hand, a peptide vaccine was
designed to raise antibodies against the C-terminal of αSyn in mice but reduced motor
activity accompanied by degeneration of dopaminergic neurons. Therefore, the applicant
of active immunization against αSyn C-terminal should be exercised with caution.
會後合照
更新 : 2022-10-23
