Alzheimer’s disease (AD) is the leading cause of dementia. The majority of AD cases are late-onset, multifactorial cases. Genome-wide association studies have identified more than 30 loci associated with sporadic AD (SAD), one of which is Bridging integrator 1 (BIN1). For the past few years, there has been a consensus that BIN1 is second only to APOE as the strongest genetic risk factor for SAD. Therefore, many researchers have put great effort into studying the mechanism by which BIN1 might be involved in the pathogenetic process of AD. To date, plenty of evidence has shown that BIN1 may participate in several pathways in AD, including tau and amyloid pathology. In addition, BIN1 has been indicated to take part in other relevant pathways such as inflammation, apoptosis, and calcium homeostasis. In this review, we systemically summarize the research progress on how BIN1 participates in the development of AD, with the expectation of providing promising perspectives for future research.

阿尔茨海默病 (AD) 是导致痴呆的主要原因。大多数 AD 病例是迟发性多因素病例。全基因组关联研究已经确定了 30 多个与散发性 AD (SAD) 相关的位点，其中之一是 Bridging integrator 1 ( BIN1 )。在过去的几年中，人们一致认为BIN1是仅次于APOE的 SAD 最强遗传风险因素。因此，许多研究人员致力于研究BIN1可能参与AD发病过程的机制。迄今为止，大量证据表明BIN1可能参与 AD 的多种途径，包括 tau 和淀粉样蛋白病理学。此外，BIN1已表明参与其他相关途径，如炎症、细胞凋亡和钙稳态。在这篇综述中，我们系统地总结了BIN1如何参与AD发展的研究进展，以期为未来的研究提供有希望的前景。