β-Amyloid (1-42), human TFA

Amyloid β-Peptide (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, Simões 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.