β-Amyloid 22-35 (Amyloid β-Protein (22-35)) is a 14-amino acid peptide fragment that can spontaneously aggregate to form β-sheet structures and exerts significant cytotoxicity on hippocampal neurons[1-2]. β-Amyloid 22-35 is applicable for studying the pathological mechanisms of Alzheimer's disease (AD), constructing drug screening models, and investigating related neurodegenerative diseases[3-4].
In vitro, β-Amyloid 22-35 (10–40μg/mL) was applied to cultured rat hippocampal neurons under serum-deprived conditions for 3 days. β-Amyloid 22-35 induced cytotoxicity, characterized by neurite fragmentation and increased lactate dehydrogenase release[5].
In vivo, β-Amyloid 22-35 (4nmol in 4μL; single injection) was administered to mice via intracerebroventricular injection. β-Amyloid 22-35 was shown to induce hippocampal neuronal damage and lead to learning and memory dysfunction, as evidenced by prolonged latencies in water maze tests and impaired escape responses in shuttle box tests[6].
References:
[1] Chauhan V, Sheikh AM, Chauhan A, et al. Fibrillar amyloid beta-protein inhibits the activity of high molecular weight brain protease and trypsin. J Alzheimers Dis. 2005 Feb;7(1):37-44.
[2] Fawver JN, Duong KT, Wise-Scira O, et al. Probing and trapping a sensitive conformation: amyloid-β fibrils, oligomers, and dimers. J Alzheimers Dis. 2012;32(1):197-215.
[3] Yousefirad N, Kaygısız Z, Aydın Y. Amyloid beta peptide 22-35 induces a negative inotropic effect on isolated rat hearts. Int J Physiol Pathophysiol Pharmacol. 2016 Dec 25;8(4):146-151.
[4] Di Scala C, Yahi N, Lelièvre C, et al. Biochemical identification of a linear cholesterol-binding domain within Alzheimer's β amyloid peptide. ACS Chem Neurosci. 2013 Mar 20;4(3):509-17.
[5] Takadera T, Sakura N, Mohri T, et al. Toxic effect of a beta-amyloid peptide (beta 22-35) on the hippocampal neuron and its prevention. Neurosci Lett. 1993 Oct 14;161(1):41-4.
[6] Zhao BQ, Guo YR, Li XL, et al. Amelioration of dementia induced by Aβ 22-35 through rectal delivery of undecapeptide-hEGF to mouse brain. Int J Pharm. 2011 Feb 28;405(1-2):1-8.
β-Amyloid 22-35 (Amyloid β-Protein (22-35))是一种由14个氨基酸组成的多肽片段，能够自发聚集形成β-折叠结构，并对海马神经元产生显著的细胞毒性作用[1-2]。β-Amyloid 22-35可用于阿尔茨海默病（AD）的病理机制研究、药物筛选模型构建及相关神经退行性疾病的研究[3-4]。
在体外，β-Amyloid 22-35（10–40μg/mL）作用于大鼠海马神经元培养体系（血清缺失条件下处理3天）。β-Amyloid 22-35可引发细胞毒性，包括神经元突触断裂和乳酸脱氢酶释放增加[5]。
在体内，β-Amyloid 22-35（4nmol；4μL；单次注射）侧脑室注射处理小鼠，β-Amyloid 22-35可诱导海马神经元损伤并导致学习记忆功能障碍，表现为水迷宫和穿梭箱测试中潜伏期延长及逃避反应能力下降[6]。