Cell lines

Embryonic rat hippocampal cells

Preparation method

The solubility of this peptide in sterile water is >0.5mg/ml. Stock solution should be splited and stored at -80℃ for several months.

Reaction Conditions

20 μM, 6 hours

Applications

To investigate the involvement of the tau phosphorylation kinases in Aβ (25–35)-induced tau phosphorylation, the level of each kinase was determined after Aβ (25–35) (20μM) exposure for various periods. GSK-3α did not show a significant change in response to Aβ (25–35), whereas MAP kinase decreased to ~ 60% of the control after 6h Aβ (25–35) exposure, when tau was phosphorylated maximally. TPK I/GSK-3βrapidly increased in response to Aβ (25–35), reaching a maximum (2.2-fold the control) at 6 h.

Animal models

Male Charles River Wistar rats

Dosage form

Intraperitoneal injection, 400 mg/kg

Applications

A statistically significant decrease in basal ACh release (-28%) was detected one week after the injection of Aβ (25–35). The effect persisted for only two week. K+-stimulated ACh release was similarly affected by the treatment. Aβ (25–35) treatment induced a statistically significant decrease in the stimulated release on day 14 after lesioning (-45%).

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met

Amyloid- β (Aβ) peptide is commonly found in human Alzheimer’s disease (AD) brain and is the main component of Alzheimer amyloid plaques. The predominant forms of Aβ in the human brain are Aβ (1-40) and Aβ (1-42). However, the Aβ (25-35) fragment, which is physiologically present in elderly people, is the more toxic region and has recently been found to play a relevant role in AD due to its peculiar aggregation properties¹.

Aβ (25-35) is regarded to be the functional domain of Aβ, responsible for its neurotoxic properties^2-5. It represents the actual biologically active region of Aβ6. Administration of Aβ (25-35) has been shown to lead to amnesia in mice, causing impairments of spatial working memory along with the degradation of passive avoidance reactions^2-5.

In vivo, Aβ (25-35) is present in neurons of subiculum and entorhinal cortex of AD brains⁷. It is also observed in Inclusion-Body Myositis (IBM) muscle⁸.

References:
1. Millucci L, Ghezzi L, Bernardini G, Santucci A (2010) Conformations and biological activities of amyloid beta peptide 25–35. Curr Protein Pept Sc 11: 54–67.
2. Stepanichev, M.Y.; Moiseeva, Y.V.; Lazareva, N.A.; Gulyaeva,N.V. Studies of the effects of fragment (25-35) of beta-amyloid peptide on the behavior of rats in a radial maze. Neurosci. Behav. Physiol., 2005, 35(5), 511-8.
3. Limón, I.D.; Díaz, A.; Mendieta. L.; Chamorro, G.; Espinosa, B.; Zenteno, E.; Guevara, J. Amyloid-beta(25-35) impairs memory and increases NO in the temporal cortex of rats. Neurosci. Res., 2009,63(2), 129-137.
4. Pike, C. J.; Burdick, D.; Walencewicz, A. J.; Glabe, C. G.; Cotman, C. W. Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state. J. Neurosci., 1993, 13, 1676-1687.
5. Stepanichev, M.Yu; Lazareva N.A.; Onufriev, M.V.; Mitrokhina, O.S.; Moiseeva, Yu.V.; Gulyaeva, N.V. Effects of doses of fragment (25-35) of beta-amyloid peptide on behavior in rats. Neurosci. Behav. Physiol., 1998, 28(5), 564-6 .
6. D'Errico, G.; Vitiello, G.; Ortona, O.; Tedeschi, A.; Ramunno, A. and D'Ursi, A.M. Interaction between Alzheimer's A(25-35) peptide and phospholipid bilayers: The role of cholesterol. Biochimica. Biophys. Acta (BBA) – Biomembr., 2008, 1778, 2710-2716.
7. Kaneko, I.; Yamada, N.; Usui, Y.; Oda, T. Possible involvement of β -amyloids racemized at Ser residue in Alzheimer’s disease. Alzheimer’s Disease: Biology, Diagnose and Therapeutics. John Wiley & Sons: Chichester, 1997, pp. 519-528.
8. Kaneko, I.; Kubo, T.; Morimoto, K.; Kumagae, Y.; Miller, C.A. Ananimal model for Alzheimer’s disease using racemic