HK$400 for any 40µg Neuroscience Antibodies from GenScript
GenScript offers a wide selection of neuroscience antibodies for Alzheimer’s disease research as well as pathways that may play a role in Parkinson’s disease, and amyotrophic lateral sclerosis.
- Unique collection of phospho-specific antibodies and their non-phospho pairs
- Full coverage of neurological disease pathways
- Multiple applications: Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC), ELISA, etc
Terms and conditions:
1. The promotion is valid for HK & Macau customers until 12-May-2017
2. Use promotion code 2017NEURO40 when placing order with ATCG
3. Buy 3 antibodies to waive the shipping fee
Amyloid β-protein (Aβ42) oligomerization is an early event in Alzheimer’s disease (AD). Current diagnostic methods using sequence-specific antibodies against less toxic fibrillar and monomeric Aβ42 run the risk of overdiagnosis. Hence, conformation-specific antibodies against neurotoxic Aβ42 oligomers have garnered much attention for developing more accurate diagnostics. Antibody 24B3, highly specific for the toxic Aβ42 conformer that has a turn at Glu22 and Asp23, recognizes a putative Aβ42 dimer, which forms stable and neurotoxic oligomers more potently than the monomer. 24B3 significantly rescues Aβ42-induced neurotoxicity, whereas sequence-specific antibodies such as 4G8 and 82E1, which recognizes the N-terminus, do not. The ratio of toxic to total Aβ42 in the cerebrospinal fluid of AD patients is significantly higher than in control subjects as measured by sandwich ELISA using antibodies 24B3 and 82E1. Thus, 24B3 may be useful for AD diagnosis and therapy.
Monoclonal antibody with conformational specificity for a toxic conformer of amyloid β42 and its application toward the Alzheimer’s disease diagnosis. Murakami K et al. Sci Rep. 2016 Jul 4;6:29038 PMID: 27374357
#27709 Human Amyloidβ Toxic Oligomer Assay Kit – IBL is developed using the antibody (clone: 24B3) specifically detects a toxic Amyloid Beta conformer. It measures selectively putative Amyloid Beta Oligomer in CSF.
A research team led by Prof Nancy Ip of HKUST found that interleukin-33 (IL-33) ameliorates cognitive decline and Alzheimer’s disease-like pathology. The groundbreaking study has just been published in PNAS.
Defects in the removal of Aβ protein in the brain are believed to be one of the major causes underlying AD. The team at HKUST showed that the presence of IL-33 mobilized the immune cells of the brain, the microglia, to the amyloid plaques and promoted the clearance of Aβ protein. IL-33 also triggered changes in the microglia to reduce overall inflammation in the brain. Inflammation contributes to and drives the pathology of the disease.
“These exciting findings bring us one step closer to understanding the pathological process of this complex, multi-factorial disease and provide a new avenue for developing AD treatments,” said Prof Ip. “The next step will be to translate the findings from the mouse study into clinical treatments for humans.”
Amy K. Y. Fu, Kwok-Wang Hung, Michael Y. F. Yuen, Xiaopu Zhou, Deejay S. Y. Mak, Ivy C. W. Chan, Tom H. Cheung, Baorong Zhang, Wing-Yu Fu, Foo Y. Liew, and Nancy Y. Ip. (2016) IL-33 ameliorates Alzheimer’s disease-like pathology and cognitive decline. Proc Natl Acad Sci USA doi: 10.1073/pnas.1604032113.