Amyloid β-Peptide (10-20) (human)

在阿尔茨海默病（AD）中，β-淀粉样蛋白(Aβ）可以引发神经退行性病变 1。在非正常生理条件下，由β淀粉样前体蛋白(β-amyloid precursor protein,APP)水解产生，是一种分解代谢副产物2。

Aβ是许多不同受体和其它分子的配体3-5，通过复杂转运通路在组织和血脑屏障中运输。Aβ响应于各种不同的环境压力，能够诱导促炎活性⁷。

可溶性β淀粉样多肽片段是明胶酶A/ IV型胶原酶/MMP-2及APP分泌酶的底物，作用于Lys16和Leu17之间，使蛋白断裂。

参考文献：

1. Small, D.H., Mok, S.S. & Bornstein, J.C. Alzheimer’s disease and Aβ-toxicity: From top to bottom. Nature Rev. Neurosci. 2, 595–598 (2001)

2. Soscia SJ, Kirby JE, Washicosky KJ, Tucker SM, Ingelsson M, Hyman B, Burton MA, Goldstein LE, Duong S, Tanzi RE, Moir RD (2010). Bush, Ashley I.. ed. The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide. PLoS ONE 5 (3)

3. Le Y, Gong W, Tiffany HL, Tumanov A, Nedospasov S, et al. (2001) Amyloid (b)42 activates a G-protein-coupled chemoattractant receptor, FPR-like-1.J Neurosci 21: RC123.

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6. Tanzi RE, Moir RD, Wagner SL (2004) Clearance of Alzheimer’s Ab peptide: the many roads to perdition. Neuron 43: 605–608.

7. Paris D, Town T, Parker TA, Tan J, Humphrey J, et al. (1999) Inhibition of Alzheimer’s b-amyloid induced vasoactivity and proinflammatory response in microglia by a cGMP-dependent mechanism. Exp Neurol 157: 211–221.