Amyloid Beta

In addition to our program targeting the oligomerization of alpha-synuclein for treating Parkinson’s disease we have a similar program aimed at developing compounds which prevent the formation of toxic aggregates of amyloid-beta. Misfolding and aggregation of this protein plays a key role in the pathology of Alzheimer’s disease. Our efforts to target amyloid beta have resulted in the discovery of a series of compounds that prevent the aggregation of amyloid-beta in cell based assays. Initial studies in animal models suggest that these (NPT400 series) compounds have beneficial actions on neuropathology in the appropriate transgenic animal models.

APP Transgeneic Amyloid Beta
Amyloid-beta (Aβ) deposits are not normally found in the brains of non-transgenic mice (left). Transgenic mice overexpressing amyloid precursor protein (APP) develop cortical and hippocampal Aβ deposits similar to those found in the brains of Alzheimer‘s disease patients (middle). Treatment with an Aβ stabilizer decreases the number of Aβ deposits in transgenic APP mice (right).