Alzheimer's disease (AD) research ELISA kits

Alzheimer's disease (AD) research ELISA kits

Alzheimer's disease (AD) was first reported by A. Alzheimer, a German neuropathologist in 1907 and is considered as a major factor of dementia. It is known that Amyloid β (Aβ; which is major constituent of senile plaque) is cleaved from Amyloid Precursor Protein (APP; which exists in three main isoforms, APP695, APP751, and APP770) by β-secretase and subsequent γ-secretase . The production of soluble APPβ (sAPPβ) by β-secretase cleavage corresponds to Aβ production accordingly, so it is desired to measure sAPPβ in parallel with Aβ. 
In addition, it is reported that APP gene mutation exists in early-onset familial Alzheimer's disease patient. Swedish mutation, one of the APP gene mutations, is a double mutation at positions -1 to -2 from the β-secretase cleavage site (Lys670→Asn and Met671→Leu). And further, it is reported that Swedish mutation elevates Aβ40 and Aβ42 production , and that the mutation is utilized in establishment of transgenic mice . 
The measuring sAPPβ in Swedish type is useful for research of AD as well as in wild type. On the one hand, it is considered that in the metabolic pathway of APP, APP is first cleaved by α-secretase rather than β-secretase normally to produce soluble APPα (sAPPα) and subsequently P3 is cleaved from the remaining C-terminal fragment by γ-secretase. In recent research, there are several attempts to apply the inhibitor of β-secretase and the activation of α-secretase for AD treatment.