β-Amyloid (1-42), human TFA is a 42-amino acid peptide. Alzheimer's disease (AD) is characterized phenotypically by memory impairment, neurochemically by accumulation of β-amyloid peptide (such as β-Amyloid (1-42)) and morphologically by an initial loss of nerve terminals in cortical and hippocampal regions [1]. the abnormal production of soluble forms of β-amyloid peptides (Aβ), such as β-Amyloid (1-42), have been proposed as a major culprit in AD [2].
β-Amyloid (1-42) can impair synaptic function, typified by its ability to affect synaptic plasticity [3], and trigger events leading to a loss of viability of synapses [4], and leads to memory impairment [5]. The intracerebroventricular administration of β-Amyloid (1-42) has been proposed as a model of AD [6].
β-Amyloid (1-42) (100 μg/ml) for 24 h cell viability ofSH-SY5Y cells dropped to about 50%, β-Amyloid (1-42)-induced cell apoptosis could be completely prevented by EGb761 at 100 μg/ml and to a lesser extent, by quercetin (1.5 μg/ml) and ginkgolide B (10 μg/ml) [7].
β-Amyloid (1-42) (icv. 2 nmol in 4 μl) caused a predominant loss of glutamatergic and cholinergic markers [1].β-Amyloid (1-42) was combined with inducers of oxidative stress to induce neuronal cell death, amyloid deposits, gliosis and memory impairment following a 4 week intracerebroventricular infusion. Oxidative stress was induced using the pro-oxidative cation Fe2+ and the glutathione synthesis inhibitor buthionine sulfoximine (BSO) [8].
References:
[1].Canas P M, Sim?es A P, Rodrigues R J, et al. Predominant loss of glutamatergic terminal markers in a β-amyloid peptide model of Alzheimer's disease[J]. Neuropharmacology, 2014, 76: 51-56.
[2].Hardy J, Selkoe D J. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics[J]. science, 2002, 297(5580): 353-356.
[3].Venkitaramani D V, Chin J, Netzer W J, et al. β-amyloid modulation of synaptic transmission and plasticity[J]. Journal of Neuroscience, 2007, 27(44): 11832-11837.
[4].Mattson M P, Partin J, Begley J G. Amyloid β-peptide induces apoptosis-related events in synapses and dendrites[J]. Brain research, 1998, 807(1-2): 167-176.
[5].Selkoe D J. Soluble oligomers of the amyloid β-protein: Impair synaptic plasticity and behavior[J]. Synaptic Plasticity and the Mechanism of Alzheimer's Disease, 2008: 89-102.
[6].Lawlor P A, Young D. Aβ infusion and related models of Alzheimer dementia[M]//Animal models of Dementia. Humana Press, 2011: 347-370.
[7].Shi C, Zhao L, Zhu B, et al. Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against β-amyloid peptide-induced toxicity in SH-SY5Y cells[J]. Chemico-biological interactions, 2009, 181(1): 115-123.
[8].Lecanu, L., Greeson, J., & Papadopoulos, V. (2006). Beta-amyloid and oxidative stress jointly induce neuronal death, amyloid deposits, gliosis, and memory impairment in the rat brain. Pharmacology, 76(1), 19-33.
β-Amyloid (1-42), human TFA淀粉样蛋白 β 肽 (1-42) 人 TFA 是一种由 42 个氨基酸组成的肽。阿尔茨海默氏病 (AD) 的表型特征是记忆障碍,神经化学特征是 β-淀粉样肽（例如 β-淀粉样蛋白 (1-42)）的积累,形态特征是皮层和海马区域神经末梢的初始丧失 [ 1]。 β-淀粉样蛋白 (1-42) 等可溶性形式的 β-淀粉样肽 (Aβ) 的异常生成被认为是 AD [2] 的罪魁祸首。
β-淀粉样蛋白 (1-42) 可损害突触功能,其典型特征是其影响突触可塑性的能力[3],并触发导致突触活力丧失的事件[ 4],并导致记忆障碍[5]。脑室内注射β-淀粉样蛋白（1-42）已被提议作为AD的模型[6]。
β-淀粉样蛋白 (1-42) (100 μg/ml) 24 小时后,SH-SY5Y 细胞的细胞活力下降至约 50%,β-淀粉样蛋白 (1-42) 诱导的细胞凋亡可被 EGb761 完全阻止100 μg/ml 和较小程度的槲皮素 (1.5 μg/ml) 和银杏内酯 B (10 μg/ml) [7]。
β-淀粉样蛋白 (1-42)（icv. 2 nmol in 4 μl）导致谷氨酸能和胆碱能标记物的主要损失[1]。β-淀粉样蛋白 (1-42) 结合在 4 周的脑室内输注后,用氧化应激诱导剂诱导神经元细胞死亡、淀粉样蛋白沉积、神经胶质增生和记忆障碍。使用促氧化阳离子 Fe2+ 和谷胱甘肽合成抑制剂丁硫氨酸亚砜亚胺 (BSO) [8] 诱导氧化应激。