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.
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.
|Davtyan, Hayk; Ghochikyan, Anahit; Hovakimyan, Armine et al. (2014) Immunostimulant patches containing Escherichia coli LT enhance immune responses to DNA- and recombinant protein-based Alzheimer's disease vaccines. J Neuroimmunol 268:50-7|
|Evans, Claire F; Davtyan, Hayk; Petrushina, Irina et al. (2014) Epitope-based DNA vaccine for Alzheimer's disease: translational study in macaques. Alzheimers Dement 10:284-95|
|Kwapis, Janine L; Wood, Marcelo A (2014) Epigenetic mechanisms in fear conditioning: implications for treating post-traumatic stress disorder. Trends Neurosci 37:706-20|
|Davtyan, Hayk; Ghochikyan, Anahit; Petrushina, Irina et al. (2014) The MultiTEP platform-based Alzheimer's disease epitope vaccine activates a broad repertoire of T helper cells in nonhuman primates. Alzheimers Dement 10:271-83|
|Ghochikyan, Anahit; Petrushina, Irina; Davtyan, Hayk et al. (2014) Immunogenicity of epitope vaccines targeting different B cell antigenic determinants of human *-synuclein: feasibility study. Neurosci Lett 560:86-91|
|Vogel-Ciernia, Annie; Matheos, Dina P; Barrett, Ruth M et al. (2013) The neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory. Nat Neurosci 16:552-61|
|Bullain, Szofia S; Corrada, Maria M; Shah, Barbara Agee et al. (2013) Poor physical performance and dementia in the oldest old: the 90+ study. JAMA Neurol 70:107-13|
|Poon, Wayne W; Blurton-Jones, Mathew; Tu, Christina H et al. (2011) ?-Amyloid impairs axonal BDNF retrograde trafficking. Neurobiol Aging 32:821-33|
|Davtyan, H; Mkrtichyan, M; Movsesyan, N et al. (2010) DNA prime-protein boost increased the titer, avidity and persistence of anti-Abeta antibodies in wild-type mice. Gene Ther 17:261-71|
|Corrada, Maria M; Brookmeyer, Ron; Paganini-Hill, Annlia et al. (2010) Dementia incidence continues to increase with age in the oldest old: the 90+ study. Ann Neurol 67:114-21|
Showing the most recent 10 out of 79 publications