Amyloid Beta-peptide (25-35) (human) |
| Catalog No.GP10082 |
Amyloid beta-peptide (25-35) (human) is an fragment of Alzheimer's Amyloid beta peptide which has neurotoxic effects.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 131602-53-4
Sample solution is provided at 25 µL, 10mM.
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Amyloid beta(Aβ)-peptide (25-35) (human) is an fragment of Alzheimer's Amyloid beta peptide which is commonly found in the brains of people with Alzheimer's disease (AD) and is a major component of Alzheimer's amyloid plaques[1-3]. Amyloid beta-peptide (25-35) (human) is considered a functional domain of Aβ due to its neurotoxic effects, and it is the bioactive region of beta-amyloid[4].
Amyloid beta-peptide (25-35) (human) treatment (20 μM, 6 hours) activated tau protein kinase I/glycogen synthase kinase-3beta (TPKI/GSK-3beta) in primary culture of hippocampal neurons [5]. The Amyloid beta-peptide (25-35) (human) (100nM, 1μM, 10μM, or 30μM) reduces the viability of cultured cerebral cortical rat neurons [6]. Amyloid beta-peptide (25-35) (human) (10μM) increased the amplitude of excitatory responses produced by local iontophoretic applications of glutamate and NMDA [7]. Treatment of PC12 cells with 20 μM of Amyloid beta-peptide (25-35) (human) for 24 h induced cytotoxicity as the cell viability was reduced to 67% of the control value (100%)[8].
A single intracerebroventricular (i.c.v.) injection of Amyloid beta-peptide (25-35) (human) (15 nmol/5 μl; i.c.v.;8days) at a dose of 15 nmol/rat induced a marked decrease in latency in step-through passive avoidance task[9].
References:
[1]. Nalbantoglu J. Beta-amyloid protein in Alzheimer's disease. Can J Neurol Sci. 1991 Aug;18(3 Suppl):424-7. doi: 10.1017/s0317167100032595. PMID: 1933692.
[2]. Rush DK, Aschmies S, et,al. Intracerebral beta-amyloid(25-35) produces tissue damage: is it neurotoxic? Neurobiol Aging. 1992 Sep-Oct;13(5):591-4. doi: 10.1016/0197-4580(92)90061-2. PMID: 1281289.
[3]. Mattson MP, Cheng B, et,al. beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity. J Neurosci. 1992 Feb;12(2):376-89. doi: 10.1523/JNEUROSCI.12-02-00376.1992. PMID: 1346802; PMCID: PMC6575616.
[4]. D'Errico, G; Vitiello, G; et,al. Interaction between Alzheimer's A(25-35) peptide and phospholipid bilayers: The role of cholesterol. Biochimica. Biophys. Acta (BBA) – Biomembr., 2008, 1778, 2710-2716.
[5]. Takashima A, Honda T, et,al. Activation of tau protein kinase I/glycogen synthase kinase-3beta by amyloid beta peptide (25-35) enhances phosphorylation of tau in hippocampal neurons. Neurosci Res. 1998 Aug;31(4):317-23. doi: 10.1016/s0168-0102(98)00061-3. PMID: 9809590.
[6]. Wang Y, Liu L, et,al. Mechanism of soluble beta-amyloid 25-35 neurotoxicity in primary cultured rat cortical neurons. Neurosci Lett. 2016 Apr 8;618:72-76. doi: 10.1016/j.neulet.2016.02.050. Epub 2016 Mar 3. PMID: 26940239.
[7]. Carette B, Poulain P, et,al. Electrophysiological effects of 25-35 amyloid-beta-protein on guinea-pig lateral septal neurons. Neurosci Lett. 1993 Mar 5;151(1):111-4. doi: 10.1016/0304-3940(93)90059-t. PMID: 8385758.
[8]. Xian YF, Lin ZX, Mao QQ, Ip SP, Su ZR, Lai XP. Protective effect of isorhynchophylline against β-amyloid-induced neurotoxicity in PC12 cells. Cell Mol Neurobiol. 2012 Apr;32(3):353-60. doi: 10.1007/s10571-011-9763-5. Epub 2011 Nov 1. PMID: 22042506.
[9]. Yamaguchi Y, Kawashima S. Effects of amyloid-beta-(25-35) on passive avoidance, radial-arm maze learning and choline acetyltransferase activity in the rat. Eur J Pharmacol. 2001 Feb 2;412(3):265-72. doi: 10.1016/s0014-2999(01)00730-0. PMID: 11166290.
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