项目来源
芬兰研究理事会基金(AKA)
项目主持人
未公开
项目受资助机构
Itä-Suomen yliopisto
项目编号
27075
立项年度
2020
立项时间
未公开
研究期限
未知 / 未知
项目级别
国家级
受资助金额
262004.00欧元
学科
Biomedicine
学科代码
未公开
基金类别
Research Council of Finland-Post Doctoral Researcher
关键词
Biolääketieteet ; tutkimus ; Alzheimerin tauti ; geenit ; muutos ; ikääntyminen ; research ; Alzheimer's disease ; genes ; change ; ageing ; proteins ; molecular proteins
参与者
未公开
参与机构
未公开
项目标书摘要：This research project elucidates how recently identified variant in microglia-specific PLCG2 gene(P522R,protective variant)is associated with molecular,cellular,pathophysiological and behavioral aspects of aging and Alzheimer's disease(AD).State-of-the-art in vitro and in vivo models and techniques in combination with up-to-date methodologies will be used to facilitate mechanistic characterization of the variant.It is expected that untangling the protective action(s)exerted by the variant will shed light into the role of microglia and immune system upon aging and AD-associated cellular stress.Furthermore,it is expected that the project pinpoints new therapeutic targets and paves the way for potential treatment strategies,which are based on PLC?2-related modulation of microglia in AD and in other neurodegenerative diseases involving altered immune system function.
Application Abstract: This research project elucidates how recently identified variant in microglia-specific PLCG2 gene(P522R,protective variant)is associated with molecular,cellular,pathophysiological and behavioral aspects of aging and Alzheimer's disease(AD).State-of-the-art in vitro and in vivo models and techniques in combination with up-to-date methodologies will be used to facilitate mechanistic characterization of the variant.It is expected that untangling the protective action(s)exerted by the variant will shed light into the role of microglia and immune system upon aging and AD-associated cellular stress.Furthermore,it is expected that the project pinpoints new therapeutic targets and paves the way for potential treatment strategies,which are based on PLC?2-related modulation of microglia in AD and in other neurodegenerative diseases involving altered immune system function.
