實驗室名稱：神經退化標誌研究室
主持人：林詠峯老師
許多先進國家或地區包括台灣，因人口老化和環境污染等問題，導致神經退化性失智如阿茲海默症的影響日益嚴重。根據統計，全台目前的失智人口約百分之一，估計二十年後會超過百分之三。已知類澱粉胜肽的產生以致在腦中堆積是這類神經退化的主因，因此本研究室利用細胞和小鼠等實驗模型，以及檢測臨床病人血液中成份，探討神經退化中與類澱粉前驅蛋白的囊泡運輸相關之致病機轉、生物標誌、以及使用醣苷神經鞘醯胺類藥物、人參廢料萃取物等之療效和安全性評估，研究成果可作為將來臨床試驗的準備；不僅可以促進病人福祉，也減低家屬和社會的負擔。
Research goal
The microtubule-based vesicle transport machinery containing motor proteins, namely dynein/dynactin and kinesin, and adaptors, AHI1 and HAP1, is vital for neuronal survival by delivering neurotrophic cargos such as APP and Trk. Gangliosides may surround APP and other neurotrophic receptors and affect their vesicular transport via HAP1/AHI1-interacting proteins. The level and modification of these proteins could serve as biomarkers for early diagnosis and treatment of neurodegenerative diseases.
References
- Expression of AHI1 rescues amyloidogenic pathology in Alzheimer’s disease model cells. Mol Neurobiol. 2019 May (In press)
- Ganglioside Hp-s1 analogue inhibits amyloidogenic toxicity in Alzheimer’s disease model cells. ACS Chem Neurosci. 2019 Jan 10:528-536.
- Regulation of Axonal Transport by Protein Kinases. Trends Biochem Sci. 2015 Oct 40(10):597-610
- Huntingtin associated protein 1 regulates trafficking of the amyloid precursor protein and modulates amyloid beta levels in neurons. J Neurochem. 2012 Sep 122(5):1010-22