中文摘要：

老年性痴呆症（Alzheimer’s disease，AD）一个重要的病理学特征，是在神经细胞外形成由β-淀粉样蛋白（β-amyloid，Aβ）组成的淀粉样斑（amyloidplaques）。β-淀粉样蛋白前体蛋白（β-amyloidprocursorprotein，APP）经β-分泌酶和γ-分泌酶依次水解后产生AB和APP胞内结构域（APP intrace Uulardomain，AICD）。现在已经知道AB在AD的发病机制中起着关键作用，但是关于AICD的生理及病理功能还不清楚。近年来研究发现AICD可以与细胞内多种蛋白相互作用，而且AICD在基因转录、细胞凋亡以及APP的加工和运输过程中均有调节功能。本文针对这一领域的研究进展，对AICD的生理及病理功能进行探讨。

英文摘要：

One of the neuropathologic hallmarks of Alzheimer＇s disease （AD） is the presence of senile plaques which consist of β-amyloid peptide （Aβ） in the brain. Aβ is derived from β-amyloid precursor protein （APP） through sequential cleavages by the β-secretase and the y-secretase. In addition to Aβ, γ-cleavage releases the intracellular domain of APP （AICD）. However, although it is well-established that Aβis the prime culprit for AD pathogenesis, the physio/pathological fimctions of AICD remain largely elusive. Here we.review recent progress toward elucidating the functional roles of AICD, which include modulating intracellular trafficking/processing of APP, inducing apoptosis, and regulating gene expression at transcriptional level.