Project Number 5P50AG005131-32 Agency/Funding Organization NIA Funding Year 2015 View Full Project Details for PROJECT 2: DISEASE MECHANISMS IN FRONTOTEMPORAL DEMENTIA LINKED TO C9ORF72 EXPANS 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) 5. Other Proteinopathies c. C9ORF-72 and Progranulin Category F. Research Resources 1. Alzheimer's Disease Centers Researcher and Organization Principal Investigator LAGIER-TOURENNE, CLOTILDE Principal Investigator First Name CLOTILDE Principal Investigator Last Name LAGIER-TOURENNE Awardee Organization UNIVERSITY OF CALIFORNIA SAN DIEGO Awardee State California Contact PI Country United States Project Detail Funding Opportunity Announcement RFA-AG-13-019: Alzheimer's Disease Research Centers (P50) FY Overall Cost $180,577 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
