This human Aß42 ELISA kit is to be used for the in vitro quantitative determination of human Aß42 concentrations in cell culture supernatant and other biological fluids. This kit is intended for LABORATORY RESEARCH USE ONLY.

INTRODUCTION

Alzheimer’s disease (AD) is a neurodegenerative disease that affects about 6% senior people worldwide.  It is characterized by the formation of extracellular amyloid plaques, the accumulation of neurofibrillary tangles in neurons, and loss of neurons in some area of the brain.  Amyloid beta peptide 42 (Aß42) has a tendency toward forming beta pleated structure and precipitation.  It constituents the initial and key component of the insoluble amyloid fibril in the plaque.  Aß42, like other amyloid peptides, is formed by the sequential cleavage of amyloid precursor protein by beta-secretase and gamma-secretase.  Aß40, Aß42 and Aß43 are different only at the few C-end amino acids.   Aß42 is believed to contribute to the pathogenesis of AD.  One hypothetical mechanism is that the deposition of amyloid fibril onto the brain tissue results in AD.  Another hypothesis is that the neurotoxicity of Aß42 oligomer is the cause of the disease. 

Study suggested that lower than normal Aß42/ Aß40 ratio in cerebrospinal fluid could predicate development of AD.  In blood and cerebrospinal fluid, the concentration of Aß40 is about 10 times higher than that of Aß42. 

Hyper-phosphorylated Tau protein forms neurofibrillary tangles inside neurons.  Study found that Aß42 level is lower and phosphorylated Tau protein level is higher in the cerebrospinal fluid of AD patients comparing with normal control and other dementia conditions. 

This Aß42 ELISA kit can be used for measuring Aß42 in tissue homogenate, cell culture supernatant, and other biological fluids.  The kit is for research use only, therefore, should not be used in any diagnostic or therapeutic procedures. 

CITATIONS

1. Zhao A, Li Y, Qiu Y, Li B, Xu W, Wang Y, Liu J, Deng Y.Increased prediction value of biomarker combinations for the conversion of mild cognitive impairment to Alzheimer's dementia. Transl Neurodegener 2020; 9(1):30.