sAPPβ-w (Highly Sensitive)

Solid phase sandwich ELISA for the determination human sAPPβ-w in EDTA plasma, cerebrospinal fluids and cell culture supernatant. For research use only, not for use in diagnostic procedures.<br><br>

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 individuals who suffer early-onset familial Alzheimer’s disease. 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. This kit can measure human soluble sAPPβ wild type (sAPPβ-w) in samples. IBL has many other kinds of Amyloidβ-related products for AD research. They are very specific assay systems for each target and they can be used according to the purpose of study.