This is the first oligomeric amyloid beta ELISA to take advantage of MOAB-2′s high specificity and avidity for beta amyloid peptides and combine it in a proprietary formulation that allows for the detection of amyloid beta oligomers and complexes present in mouse and human CSF and brain tissue extracts. The ELISA comes complete and ready to use with all the necessary buffers and detection reagents as well as ready-to-polymerize human Aβ 1-42 peptide standards.
Biosensis retains exclusive worldwide rights for MOAB-2 based immunoassays and this is the first of a family of critical Alzheimer’s Disease biomarker assays to be released by Biosensis for neurological disease research. Biosensis’ oAβ ELISA results match that published in the literature for AD patients and transgenic mouse models, and improves them by providing extremely low backgrounds, superb low end sensitivity, a broad dynamic range and great reproducibility.
Product Code: BEK-2215-2P
Product Name: Oligomeric Amyloid beta (oAβ) ELISA
Specificity: Human. MOAB-2 (mouse IgG2b) is a pan-specific, high-titer antibody to Aβ residues 1-4 and is highly specific to amyloid beta peptide. The Biosensis o-Aβ Elisa detects Aβ oligomers as validated and described by Youmans KL et al (2012).
Other Names: Beta-APP42; Beta-APP40; Beta-amyloid protein 42; Beta-amyloid protein 40; ABPP; APPI; Amyloid beta A4 protein; MOAB2; MOAB-2; Alzheimer’s antibody; AB40; AB42; abeta.
The ELISA kit box contains 2 x 96 pre-coated strip plates, protein standards, detection reagents, substrate buffer and precise instructions.
- low background
- low end sensitivity
- broad dynamic range
Range: 15.6 – 1000 pg/mL
Sensitivity: 30-60 pg/mL (defined as 150% of blank value)
BackgroundAlzheimer’s disease (AD) is the most common cause of dementia and accounts for 50%-75% of all cases. It has been identified as a protein misfolding disease caused by plaque accumulation of abnormally folded beta amyloid and tau amyloid proteins in the brain. Plaques are made up of small peptides, 39–43 amino acids in length, called beta-amyloid (Aβ) which is a fragment from a larger protein called amyloid precursor protein (APP), which is critical to neuron growth, survival and post-injury repair. In AD, a proteolysis process causes APP to be divided into smaller fragments  which gives rise to fibrils of beta-amyloid that deposit outside neurons in dense formations known as senile plaques.. Exactly how disturbances of production and aggregation of the beta-amyloid peptide gives rise to the pathology of AD is not known.
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