Bridging integrator 1 (BIN1): form, function, and Alzheimer's disease

被引：142

作者：

Tan, Meng-Shan ^{[1
,2
]}

Yu, Jin-Tai ^{[1
,2
]}

Tan, Lan ^{[1
,2
]}

机构：

[1] Ocean Univ China, Coll Med & Pharmaceut, Qingdao 266003, Peoples R China

[2] Qingdao Univ, Qingdao Municipal Hosp, Sch Med, Dept Neurol, Qingdao 266071, Peoples R China

来源：

TRENDS IN MOLECULAR MEDICINE | 2013年 / 19卷 / 10期

基金：

中国国家自然科学基金;

关键词：

Alzheimer's disease; BIN1; genetics; pathogenesis; tau; therapy; GENOME-WIDE ASSOCIATION; TUMOR-SUPPRESSOR BIN1; C-MYC; INDOLEAMINE 2,3-DIOXYGENASE; GENETIC ASSOCIATION; IDENTIFIES VARIANTS; AMPHIPHYSIN FAMILY; COMMON VARIANTS; ENDOCYTOSIS; PROTEIN;

D O I：

10.1016/j.molmed.2013.06.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The bridging integrator 1 (BIN1) gene, also known as amphiphysin 2, has recently been identified as the most important risk locus for late onset Alzheimer's disease (LOAD), after apolipoprotein E (APOE). Here, we summarize the known functions of BIN1 and discuss the polymorphisms associated with LOAD, as well as their possible physiological effects. Emerging data suggest that BIN1 affects AD risk primarily by modulating tau pathology, but other affected cellular functions are discussed, including endocytosis/trafficking, inflammation, calcium homeostasis, and apoptosis. Epigenetic modifications are important for AD pathogenesis, and we review data that suggests the possible DNA methylation of the BIN1 promoter. Finally, given the potential contributions of BIN1 to AD pathogenesis, targeting BIN1 might present novel opportunities for AD therapy.

引用

页码：594 / 603

页数：10

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