At present, there is no effective treatment to arrest the progression of Alzheimer disease (AD) - the most common cause of dementia affecting the elderly. The disease is caused by accumulation of two distinct clumps of proteins in the brain called neuritic plaques and neurofibrillary tangles formed by amyloid beta peptide and tau protein, respectively. Evidence suggests that increased levels and aggregation of these proteins contribute to cell death and subsequent development of AD pathology. In this study, using in vitro studies and cellular/animal models, we will evaluate the implication of a novel biomolecule called PEG-PLGA nanoparticles for the treatment of AD. Given our recent data, we believe that PEG-PLGA will attenuate aggregation/conversion of amyloid beta peptide and tau protein into toxic forms and reduce neuronal death and pathology in cellular/animal models of AD. This is a disease-modifying, translational project, which may provide a novel nanoparticle-based treatment strategy for AD patients.
