老年斑是一个多世纪前通过经典银染色方法在颞叶癫痫、阿尔茨海默病（AD）和老年无痴呆个体脑内发现的神经病理改变。1984及1985年,β-淀粉样蛋白(Aβ)从脑血管淀粉病变和老年斑中鉴定，成为老年斑发生机制以及老年性痴呆疾病现代研究的里程碑, 也推动了AD诊断和治疗领域的发展。然而，AD领域迄今遗留一个未确定的核心问题: 除Aβ, 老年斑是否含来源于其他蛋白质的沉积成分？得益于人脑组织库建设，我们最近发现分拣蛋白（sortilin）的一个降解肽段可形成纤丝状产物沉积于老年斑。基于该原始发现，我们一方面将重点拓展湘雅医学院人脑组织库建设。同时，我们将充分利用人脑组织材料，探讨分拣蛋白沉积肽段的形成原理和作为AD病理诊断的新工具和体液检测生物标记物的可能性。

Senile plaques (SPs) were originally discovered in the human brains from patients with temporal epilepsy, Alzheimer's disease (AD) and nondemented elderly using classic silver stains over a century ago. In 1984 and 1985, beta-amyloid peptide (Aβ) was identified as a component of the amyloid material in cerebral vascular angiopathy and SPs, marking the milestone in modern research into plaque pathogenesis and age-related dementia, including the development of diagnostic and therapeutic approaches for AD. However, a central question remains scarcely investigated to date is whether there are other protein products, besides Aβ, that also deposit at SPs. Using postmortem brains from Chinese donors, we have recently discovered that a peptide derived from sortilin forms extracellular fibrillary deposits at cerebral SPs. We will expand our human brain banking program and use the human brain samples to explore the mechanism underlying sortilin proteolysis and formation of its fibrillary fragments, as well as the possibility of using fragments as potential diagnostics and biomarkers for AD.