Project Number 5P01AG010435-21 Agency/Funding Organization NIA Funding Year 2014 View Full Project Details for Neprilysin Modification of Amyloid Processing in Models of AD Research Categorization Primary Disease / Condition Alzheimer's Disease CADRO Category A. Molecular Pathogenesis and Physiology of Alzheimer's Disease and Alzheimer's Disease-related Dementias (AD/ADRDs) 1. Amyloid beta f. Amyloid beta Structure, Assembly, and Aggregation Researcher and Organization Principal Investigator TUSZYNSKI, MARK H. Principal Investigator First Name MARK H. Principal Investigator Last Name TUSZYNSKI Awardee Organization UNIVERSITY OF CALIFORNIA SAN DIEGO Awardee State California Contact PI Country United States Project Detail FY Overall Cost $253,715 Funding Organization Agency/Funding Organization NIA Funding Organization Country United States Program Official BUCKHOLTZ, NEIL Related Resources Repository [AlzPED] Novel therapeutic strategy for neurodegeneration by blocking Aβ seeding mediated aggregation in models of Alzheimer's disease. [AlzPED] Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic models. [AlzPED] A Neuroprotective Brain-penetrating Endopeptidase Fusion Protein Ameliorates Alzheimer Disease Pathology and Restores Neurogenesis [AlzPED] Early BDNF treatment ameliorates cell loss in the entorhinal cortex of APP transgenic mice. [AlzPED] Neuroprotective effects of regulators of the glycogen synthase kinase-3beta signaling pathway in a transgenic model of Alzheimer's disease are associated with reduced amyloid precursor protein phosphorylation.