Mouse Aβ1-42(Amyloid Beta 1-42) ELISA Kit (E-EL-M3010)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Mouse Aβ1-42. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Mouse Aβ1-42 and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Mouse Aβ1-42, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Mouse Aβ1-42. You can calculate the concentration of Mouse Aβ1-42 in the samples by comparing the OD of the samples to the standard curve.

Amyloid beta 1-42 (Abeta1-42) is a 42-residue amyloid peptide generated from the amyloid beta precursor protein (APP) by sequential cleavage with beta-secretase and gamma-secretase. Cleavage by alpha-secretase within the amyloid region precludes formation of intact Abeta, so the balance among these processing routes determines how much aggregation-prone peptide is produced. In the amyloidogenic pathway beta-secretase first releases a soluble N-terminal ectodomain and leaves a membrane-anchored C-terminal stub, which gamma-secretase then cleaves within the transmembrane region to liberate Abeta peptides, principally the 40- and 42-residue forms. The additional hydrophobic residues at the C-terminus make Abeta1-42 self-associate far more readily, and it is regarded as a principal constituent of the extracellular senile plaques characteristic of Alzheimer-type neuropathology. Quantification of Abeta1-42 in brain extracts, cerebrospinal fluid and plasma is widely used in preclinical research on Alzheimer disease and cerebral amyloid angiopathy, and in transgenic mouse models it reports cerebral amyloid burden and the efficacy of secretase inhibitors, gamma-secretase modulators and anti-amyloid immunotherapies. Because soluble oligomers are neurotoxic and impair synaptic plasticity before plaques appear, the Abeta1-42/Abeta1-40 ratio serves as an important index of amyloid metabolism and of shifts in gamma-secretase processivity.