基本信息
浏览量:0
职业迁徙
个人简介
Research Interests
Inflammation is now believed to be a common mechanism of disease. Neuroinflammation, the inflammatory response that occurs in the nervous system, has been implicated in many brain disorders, including epilepsy, traumatic brain injury, stroke, and neurodegenerative diseases such as multiple sclerosis, Parkinson’s and Alzheimer’s diseases. However, our understanding of the molecular mechanisms underlying neuroinflammation in the pathogeneses of neurodegenerative diseases is still limited. My research programs focus on neuroinflammation in synaptic plasticity and neurodegenerative diseases. Specifically, I am interested in endocannabinoid and prostaglandin signaling in hippocampal synaptic plasticity and pathogenesis of Alzheimer’s disease. Recent evidence shows that a large proportion of prostaglandins derives from hydrolysis of the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) by monoacylglycerol lipase (MAGL), the enzyme that primarily metabolizes 2-AG in the brain. While 2-AG exhibits anti-inflammatory and neuroprotective properties, prostaglandins (e.g., PGE2) are proinflammatory and neurotoxic. Therefore, MAGL plays an important role in homeostatic regulation of endocannabinoid 2-AG and prostaglandin signaling (See inset) in physiology and diseases. Thus, inhibition of MAGL will result in strengthening anti-inflammatory and neuroprotective 2-AG signaling, while reducing proinflammatory arachidonic acid and prostaglandin levels. We are currently addressing this important issue as to whether inactivation of MAGL is able to impromve hippocampal synaptic plasticity, learning and memory and reduce neuropathology of Alzheimer’s disease and whether epigenetic mechanisms such as noncoding small RNAs (miRNAs) are involved in regulation of synaptic plasticity and neuropathology by endocannabinoid and prostaglandin signaling.
Inflammation is now believed to be a common mechanism of disease. Neuroinflammation, the inflammatory response that occurs in the nervous system, has been implicated in many brain disorders, including epilepsy, traumatic brain injury, stroke, and neurodegenerative diseases such as multiple sclerosis, Parkinson’s and Alzheimer’s diseases. However, our understanding of the molecular mechanisms underlying neuroinflammation in the pathogeneses of neurodegenerative diseases is still limited. My research programs focus on neuroinflammation in synaptic plasticity and neurodegenerative diseases. Specifically, I am interested in endocannabinoid and prostaglandin signaling in hippocampal synaptic plasticity and pathogenesis of Alzheimer’s disease. Recent evidence shows that a large proportion of prostaglandins derives from hydrolysis of the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) by monoacylglycerol lipase (MAGL), the enzyme that primarily metabolizes 2-AG in the brain. While 2-AG exhibits anti-inflammatory and neuroprotective properties, prostaglandins (e.g., PGE2) are proinflammatory and neurotoxic. Therefore, MAGL plays an important role in homeostatic regulation of endocannabinoid 2-AG and prostaglandin signaling (See inset) in physiology and diseases. Thus, inhibition of MAGL will result in strengthening anti-inflammatory and neuroprotective 2-AG signaling, while reducing proinflammatory arachidonic acid and prostaglandin levels. We are currently addressing this important issue as to whether inactivation of MAGL is able to impromve hippocampal synaptic plasticity, learning and memory and reduce neuropathology of Alzheimer’s disease and whether epigenetic mechanisms such as noncoding small RNAs (miRNAs) are involved in regulation of synaptic plasticity and neuropathology by endocannabinoid and prostaglandin signaling.
研究兴趣
论文共 113 篇作者统计合作学者相似作者
按年份排序按引用量排序主题筛选期刊级别筛选合作者筛选合作机构筛选
时间
引用量
主题
期刊级别
合作者
合作机构
CANCER MEDICINEno. 3 (2024): e7019-e7019
NEURAL REGENERATION RESEARCHno. 5 (2024): 955-956
Experimental neurology (2022): 114292-114292
加载更多
作者统计
合作学者
合作机构
D-Core
- 合作者
- 学生
- 导师
数据免责声明
页面数据均来自互联网公开来源、合作出版商和通过AI技术自动分析结果,我们不对页面数据的有效性、准确性、正确性、可靠性、完整性和及时性做出任何承诺和保证。若有疑问,可以通过电子邮件方式联系我们:report@aminer.cn