Loss of C9orf72 in Microglia Drives Neuronal Injury by Enhancing Synaptic Pruning in Aged and Alzheimer’s Disease Mice  

作　　者：Mengmeng Wang Yuanyuan Jiang Zhihui Huang 

机构地区：[1]School of Pharmacy,Hangzhou Normal University,Hangzhou,311121,China [2]Key Laboratory of Elemene Class Anti-Cancer Chinese Medicines,Engineering Laboratory of Development and Application of Traditional Chinese Medicines,Collaborative Innovation Center of Traditional Chinese Medicines of Zhejiang Province,Hangzhou Normal University,Hangzhou,311121,China

出　　处：《Neuroscience Bulletin》2022年第3期327-330,共4页神经科学通报（英文版）

基　　金：the National Natural Science Foundation of China(92049104 and 82103210);the Research Start-up Project by Hangzhou Normal University(4125C5021920453 and 4125C50220204106).

摘　　要：Many diseases are caused by the expansion of simple sequence repeats scattered throughout the human genome;they are defined as repeat expansion diseases.The size of the repeat unit ranges from trinucleotides(the vast majority)to tetranucleotides,pentanucleotides,hexan cleotides,and even dodecanucleotides[1].Expansions of the hexanucleotide GGGGCC in the C9orf72 gene are the most frequent genetic cause of amyotrophic lateral sclero・sis(ALS)and frontotemporal dementia(FTD)[2].In addition to ALS and FTD,C9orf72 repeat expansions may also be associated with Alzheimer's disease(AD),since the rate of such expansions in AD cases(0.57%)is higher than normal(0.11%)[3].However,the exact role of C9orf72 in AD is still unclear.

关 键 词：C9orf72 ALZHEIMER diseases 

分 类 号：R749.16[医药卫生—神经病学与精神病学]