Project Number 3P50AG005131-33S2 Agency/Funding Organization NIA Funding Year 2016 View Full Project Details for PROJECT 3: GENOMIC MOSAICISM UNDERLYING POSTERIOR CORTICAL ATROPHY (PCA) Research Categorization Primary Disease / Condition Multiple Dementias CADRO Category A. Molecular Pathogenesis and Physiology of Alzheimer's Disease and Alzheimer's Disease-related Dementias (AD/ADRDs) 17. Genetics e. Nucleic acid-related "omics" Studies Category F. Research Resources 1. Alzheimer's Disease Centers Researcher and Organization Principal Investigator CHUN, JEROLD Principal Investigator First Name JEROLD Principal Investigator Last Name CHUN Awardee Organization UNIVERSITY OF CALIFORNIA SAN DIEGO Awardee State California Contact PI Country United States Project Detail Funding Opportunity Announcement PAR-13-353: Revision Requests for Active Alzheimer's Disease Centers (P50) FY Overall Cost $243,375 Funding Organization Agency/Funding Organization NIA Funding Organization Country United States Program Official PHELPS, CREIGHTON H. Related Resources Repository [AlzPED] CRF receptor-1 antagonism mitigates Aβ pathology and cognitive and synaptic deficits in a mouse model of Alzheimer's disease [AlzPED] Peptides of presenilin-1 bind the amyloid precursor protein ectodomain and offer a novel and specific therapeutic approach to reduce ß-amyloid in Alzheimer's disease [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. [AlzPED] Cerebrolysin decreases amyloid-beta production by regulating amyloid protein precursor maturation in a transgenic model of Alzheimer's disease. [AlzPED] Amelioration of the cerebrovascular amyloidosis in a transgenic model of Alzheimer's disease with the neurotrophic compound cerebrolysin. [AlzPED] The neuroprotective effects of Cerebrolysin in a transgenic model of Alzheimer's disease are associated with improved behavioral performance. Pagination Previous page ‹‹ Page 2
