A major histopathological hallmark of Alzheimer's disease (AD) is the presence of amyloid deposits in the parenchyma of the amygdala, hippocampus, and neocortex. The principal component of amyloid is beta amyloid (AB). The pathologic accumulation of AB in plaques is postulated to result from an imbalance between production and clearance during aging. Transgenic mouse models overexpressing human amyloid precursor protein (APP) bearing certain familial AD mutations have validated overproduction of AB as driving AD-type amyloid pathology (1).
-Western-Blot-NBP2-13075-img0004.jpg "WB analysis of beta Amyloid protein.")
Advances in our understanding of the neurobiology of AD have led to the development of putative disease-modifying treatments. The most revolutionary of these approaches consists in the removal of brain beta amyloid via anti-AB antibodies (2). Immunocytochemical studies on AD transgenic mouse brains revealed abundant intraneuronal AB in brain regions which are severely affected in Alzheimer's disease resulting in extensive neuronal degeneration. Morphological and biochemical evidence as detected by anti-AB antibodies indicates that the eventual death of these cells occurs by apoptosis suggesting that AB is neurotoxic in vivo and suggests that apoptosis may be responsible for the accompanying neuronal loss, the principal underlying cellular feature of Alzheimer's disease (3). Novus Biologicals is in the forefront in offering top quality reagents to investigate the potential role of beta amyloid in the form of antibodies, lysates and RNAi products for your research needs.
Novus Biologicals offers beta amyloid reagents for your research needs including:
