报告题目：Inflammation-induced cognitive decline andprevention in obesity and metabolic syndrome 

报告人: 黄旭枫 教授，博士研究生导师，University Of Wollongong

报告时间: 2024年 10月23日星期三上午09:00

报告地点：神经科学研究所会议室401-1500

主办单位：苏州医学院   承办单位：神经科学研究所

报告人简介：

       黄旭枫，博士研究生导师，双博士学位，神经生物学博士(PhD)和科学博士(DSc)、徐州医科大学医学学士，澳大利亚新南威尔士大学医学系博士，心理学博士后，病理学博士后。于2006年取得澳大利亚终身教授，2014年任资深教授, 2018年破格晋升杰出教授。2011-2016 担任澳大利亚医学研究所（IHMRI）副所长。自1999年至今转译神经科学中心主任、代谢基础科学部主任。发表书5本，SCI国际期刊论文321篇，论文引用20,081次，H因子为75 （GS）。 曾任阿斯利康咨询顾问和澳大利亚健康医学研究理事会及生命科学专家组成员。

报告摘要：

     Today, the global obesity pandemic is a primary risk factor for metabolic syndrome (MtS). Numerous studies have linked obesity and MtS to a decline in cognitive function, yet the underlying mechanisms remain largely unclear. Our research center has explored how obesity-MtS leads to brain inflammation, subsequently resulting in excessive production of quinolinic acid, which contributes to brain injury, neurite damage, and impaired cognitive function. In examining the gut-brain axis, we discovered that the microbiota metabolite butyrate can mitigate quinolinic acid-induced cognitive decline in obesity models (Journal of Clinical Investigation, 2023). Additionally, a fiber-deficient diet was found to impair cognitive function and cause hippocampal microglia-mediated synaptic loss, mediated through the gut microbiota and its metabolites (Microbiome, 2023). Furthermore, Beta-glucan has shown promise in attenuating cognitive impairment through the gut-brain axis in diet-induced obese mice (Microbiome, 2022). In conclusion, our studies underscore the critical role of the “Gut-Brain Axis” in inflammation-induced cognitive decline. They also suggest that dietary fibers accessible to bacteria and microbiota metabolites could be pivotal in preventing or treating obesity and MtS, thereby reducing the risk of cognitive decline, type 2 diabetes, and cardiovascular diseases.