作者: Samantha L. Rosenthal , M. Ilyas Kamboh
DOI: 10.1007/S40142-014-0034-X
关键词:
摘要: Late-onset Alzheimer’s disease (LOAD) is a devastating neurodegenerative with no effective treatment or cure. In addition to APOE, recent large genome-wide association studies have identified variation in over 20 loci that contribute risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA-DRB1/HLA-DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4. addition, rare variants associated LOAD also been APP, TREM2 and PLD3 genes. Previous research has inflammatory response, lipid metabolism homeostasis, endocytosis as the likely modes through which these gene products participate disease. Despite clustering of genes across few common pathways, many their roles pathogenesis yet be determined. this review, we examine both general postulated functions consider comprehensive view potential risk.