PION/GSAP Polyclonal

Accumulation of neurotoxic amyloid-beta in the cerebral cortex is a major hallmark in the pathogenesis of Alzheimer’s disease. Formation of amyloid-beta is catalyzed by gamma-secretase, a protease with numerous substrates. PION, or GSAP, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein C-terminal fragment (APP-CTF), suggesting that PION may be a potential therapeutic target for the treatment of Alzheimer’s disease. Anti-PION antibodies are ideal for investigators involved in neuroscience research. The beta-amyloid protein precursor (APP) is cleaved by one of two beta-secretases (BACE and BACE2), producing a soluble derivative of the protein and a membrane anchored 99 -amino acid carboxy-terminal fragment (C99). The C99 fragment serves as substrate for gamma−secretase to generate the 4 kDa amyloid-beta peptide (Abeta), which is deposited in the Alzheimer’s disease patients’ brains.