Neuroscience

Alzheimer's Disease (AD)

Alzheimer’s disease (AD), the most common cause of dementia, is a progressive neurodegenerative disorder affecting more than 40 million people worldwide. 

Hallmarks are the presence of senile plaques and neurofibrillary tangles, surrounded by damaged neurons. b-Amyloid 1-42 is a major component of the plaques, and many studies suggest that it may form toxic oligomers and fibrils under physiological conditions. The pathogenic b-Amyloid 1-42 (AD) or the non-pathogenic peptide P3 (healthy individuals) are processed from the Amyloid Precursor Protein by Secretases (α, b, g).

b-secretase, but also other proteases including Glutaminyl Cyclase, Insulin Degrading Enzyme, Endothelin Converting Enzyme, Meprin b, Peptidyl Prolyl Isomerase and Neprilysin have been linked to the processing of b-Amyloid 1-42 and as such, they are considered as potential therapeutic and/or diagnostic AD targets.

Monitoring the activity of key proteases is useful in drug discovery and to screen for protease inhibitors. We constantly innovate to provide the best portfolio of quantitative assays, most being based on the FRET principle using proprietary substrates. As a world leader in FRET peptide technology we are proud to offer the same variety of long wavelength quencher and dye pairings used in our catalog peptides.

There is currently high interest in studying the aggregation process of b-Amyloids, which can be addressed using the SensoLyte® Thioflavin T β-Amyloid Aggregation Kits.

Our SensoLyte® Assay Kits enable extensive detection of protease activity to be faster, easier and compatible with HTS.