Cognitive decline and Alzheimer's disease (AD) will increase dramatically in the coming decades as the number of elderly rises from 1 out of 5 over 65 to a projected 1 out of 3 by 2050. The loss of cognitive function will impact the quality of lif, the available elderly workforce in the nation and our economic viability. We therefore urgently need to discover new prevention and treatment strategies. Biomedical research and the training of a new generation of scientists devoted to studying the mechanisms associated with aging and age-related disorders hold the greatest promise for identifying strategies that allow individuals to """"""""age successfully."""""""" Our training emphasizes preparation and instruction in the application of molecular and quantitative approaches to the elucidation of the cellular and molecular mechanisms of age-related neurodegeneration, brain plasticity, and learning and memory. Overall, our training program has 5 primary features and strengths: 1. A team of highly innovative researchers studying cutting edge questions in the field. We have 26 faculty from 11 Departments dedicated to training in areas including basic mechanism of brain dysfunction, brain plasticity and learning and memory, inflammation and inflammatory cascades, and stem cells and other therapeutics to delay and treat age-related neurological decline;2. An excellent collaborative training environment and an informative and thought provoking set of core courses, seminars, symposia and workshops;3. A mini-clinical internship for trainees to experience interacting with individuals with mild cognitive impairment (MCI) and AD and instruction and experience on brain clinical pathological case studies;4. An emphasis and training on the translation of basic research findings to humans, to reduce the incidence and progression of age-related cognitive decline and AD;and 5. Finally, individual guidance and counseling is included to optimize the potential of a diverse trainee pool and to help them realize their specific career goals. Our Program has a solid track record over its 30-year history of producing quality and highly successful scientists who enter academia or apply their training and knowledge in industry to address a challenging and serious health problem for the nation and our growing senior population.

Public Health Relevance

This renewal application seeks continued support for the training of Pre-doctoral and Post-doctoral students in the Neurobiology of Aging. Our program includes laboratory based research, formal courses and seminars, and a mini-clinic residency so that fellows literally gain training from bench to bedside. We aspire to continue to train the next generation of research scientists with an enhanced emphasis on translation of basic research findings to clinical applications in order to delay and treat age-related cognitive declin and neurodegenerative diseases.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Institutional National Research Service Award (T32)
Project #
2T32AG000096-31
Application #
8667300
Study Section
Special Emphasis Panel (ZAG1-ZIJ-3 (J1))
Program Officer
Wise, Bradley C
Project Start
1982-09-29
Project End
2019-04-30
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
31
Fiscal Year
2014
Total Cost
$392,171
Indirect Cost
$26,607
Name
University of California Irvine
Department
Internal Medicine/Medicine
Type
Organized Research Units
DUNS #
046705849
City
Irvine
State
CA
Country
United States
Zip Code
92697
Marsh, Samuel E; Yeung, Stephen T; Torres, Maria et al. (2017) HuCNS-SC Human NSCs Fail to Differentiate, Form Ectopic Clusters, and Provide No Cognitive Benefits in a Transgenic Model of Alzheimer's Disease. Stem Cell Reports 8:235-248
Carlos, Anthony J; Tong, Liqi; Prieto, G Aleph et al. (2017) IL-1? impairs retrograde flow of BDNF signaling by attenuating endosome trafficking. J Neuroinflammation 14:29
Hernandez, Michael X; Jiang, Shan; Cole, Tracy A et al. (2017) Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss. Mol Neurodegener 12:66
Marsh, Samuel E; Blurton-Jones, Mathew (2017) Neural stem cell therapy for neurodegenerative disorders: The role of neurotrophic support. Neurochem Int 106:94-100
Hernandez, Michael X; Namiranian, Pouya; Nguyen, Eric et al. (2017) C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta. ASN Neuro 9:1759091416687871
Alaghband, Yasaman; Kwapis, Janine L; López, Alberto J et al. (2017) Distinct roles for the deacetylase domain of HDAC3 in the hippocampus and medial prefrontal cortex in the formation and extinction of memory. Neurobiol Learn Mem 145:94-104
López, Alberto J; Kramár, Enikö; Matheos, Dina P et al. (2016) Promoter-Specific Effects of DREADD Modulation on Hippocampal Synaptic Plasticity and Memory Formation. J Neurosci 36:3588-99
Marsh, Samuel E; Abud, Edsel M; Lakatos, Anita et al. (2016) The adaptive immune system restrains Alzheimer's disease pathogenesis by modulating microglial function. Proc Natl Acad Sci U S A 113:E1316-25
White, André O; Kramár, Enikö A; López, Alberto J et al. (2016) BDNF rescues BAF53b-dependent synaptic plasticity and cocaine-associated memory in the nucleus accumbens. Nat Commun 7:11725
Acharya, Munjal M; Green, Kim N; Allen, Barrett D et al. (2016) Elimination of microglia improves cognitive function following cranial irradiation. Sci Rep 6:31545

Showing the most recent 10 out of 103 publications