Division of Life Science
A Stem Cell Approach to Dissect the Molecular Basis of Neurodegenerative Diseases
In 2018, this cross-institutional research project led by HKUST was awarded HK$31.2 million by the Research Grants Council under the Theme-based Research Scheme (TRS) 2018/2019 (Eighth Round). The project aims to address the urgent need for new and innovative therapies for the treatment of age-related neurodegenerative disorders, including the highly prevalent Alzheimer’s disease (AD). Recent advances in somatic cell reprograming into induced pluripotent stem cells (iPSCs) have become an opportunity for the identification of patient-specific factors to be identified, thereby, leading to advances in personalized therapy development.
Building upon a previous TRS-funded research project that identified regulatory mechanisms for the differentiation and proliferation of neural stem cells, the current project aims dissect the pathological mechanism underlying AD by employing state-of-the-art iPSC-derived platforms and CRISPR-Cas9 genome-editing technologies. To date, a total of 94 publications have resulted that have pushed our understanding of the disease. Continuation of the project will bring us one step closer to the development of novel therapies, including personalized medicine, that can ameliorate or even reverse the devastating effects of AD, thus improving the prospects of the quality of life in those affected.
First members’ meeting
First management committee meeting
RGC review visit
First annual symposium
- President
- The Morningside Professor of Life Science
- Chair Professor, Division of Life Science
- Director of State Key Laboratory of Molecular Neuroscience
科研發現
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科大突破性發現罕見腫瘤細胞「間諜」 揭示不為人知的癌細胞
香港科技大學(科大)研究人員研發了一種可為冷凍和新鮮細胞組織樣本同時進行單細胞DNA和RNA測序的新技術,更利用這方法識別出偽裝為正常細胞的罕見腦腫瘤細胞「間諜」。是次發現為一些最複雜和罕見腫瘤的研究帶來突破,並為未來的藥物靶標發現開闢新方向。
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解構秀麗隱桿線蟲pri-miRNA加工複合體的分子機制
小分子核糖核酸(microRNAs,以下簡稱miRNAs)是一種在動物和人類基因調控中發揮重要作用的小型核糖核酸(RNA),一直令許多科學家為之著迷。在生物學和醫學中,一項非常重要的研究範疇就是miRNA如何控制和調節基因表達,因為科學界一般相信,這個課題對理解細胞突變有重大作用,對於治療癌症和其他與細胞突變有關的疾病,至為關鍵。