(From the application): This training program has been developed to provide predoctoral students and postdoctoral fellows with specific training in the Neurobiology and Neuropsychology of Aging. At the core of this proposal is the merging of the expertise of investigators from two long standing NIA program projects. One is focused on human aging in health and disease (AG-04953) centered at Massachusetts General Hospital (MGH) under the direction of Dr. Marilyn Albert, one of the directors of the proposed training grant, and the other on the neural basis of cognitive decline in a non-human primate model (AG-00001) centered at Boston University School of Medicine (BUSM) of which Dr. Moss, the other director, is Co-PI. The training will focus on areas of research that include the neuropsychology and neurobiology of normal aging in humans and animal models, age-related dementia and neurologic disease; neurogenetics and neuroepidemiology; and studies of age-related changes in cellular and synaptic ultrastructure and other related topics. There are six trainers based at Boston University School of Medicine, three based at Harvard Medical School and four based at BUSM affiliated Veterans Administration Hospitals. The program includes in-depth classroom instruction, hands-on laboratory research, interactive web-site, annual field trip and retreat, and experience in one or more of the areas of the neurobiology and neuropsychology of aging being investigated by the 13 faculty. Additionally, students and fellows will attend a series of seminars on aging at BUSM and at MGH to broaden their knowledge of contemporary aging research. Trainees will also be encouraged to participate in teaching to prepare them for academic faculty positions. Class instruction for all trainees centers around the team taught introductory course in the Neurobiology and Neuropsychology of Aging, a course in Neuroscience, and a summer seminar series on Aging conducted by the Division on Aging at Harvard Medical School. These courses and seminars consist of lectures, discussions, critiques of research paper and laboratory demonstrations.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Institutional National Research Service Award (T32)
Project #
1T32AG000277-01A1
Application #
6315035
Study Section
National Institute on Aging Initial Review Group (NIA)
Program Officer
Wagster, Molly V
Project Start
2001-05-15
Project End
2006-04-30
Budget Start
2001-05-15
Budget End
2002-04-30
Support Year
1
Fiscal Year
2001
Total Cost
$153,696
Indirect Cost
Name
Boston University
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
604483045
City
Boston
State
MA
Country
United States
Zip Code
02118
Trivedi, Darshan P; Hallock, Kevin J; Bergethon, Peter R (2013) Electric fields caused by blood flow modulate vascular endothelial electrophysiology and nitric oxide production. Bioelectromagnetics 34:22-30
Kay, Kevin R; Smith, Colin; Wright, Ann K et al. (2013) Studying synapses in human brain with array tomography and electron microscopy. Nat Protoc 8:1366-80
Kopeikina, Katherine J; Wegmann, Susanne; Pitstick, Rose et al. (2013) Tau causes synapse loss without disrupting calcium homeostasis in the rTg4510 model of tauopathy. PLoS One 8:e80834
Kopeikina, Katherine J; Polydoro, Manuela; Tai, Hwan-Ching et al. (2013) Synaptic alterations in the rTg4510 mouse model of tauopathy. J Comp Neurol 521:1334-53
Kopeikina, Katherine J; Hyman, Bradley T; Spires-Jones, Tara L (2012) Soluble forms of tau are toxic in Alzheimer's disease. Transl Neurosci 3:223-233
Erb, M Kelley; Chen, Debbie K; Sassaroli, Angelo et al. (2011) Electrical stimulation of peripheral nerves induces optical responses via skeletal muscle kinematics. Proc SPIE Int Soc Opt Eng 7896:
Spires-Jones, Tara L; Kopeikina, Katherine J; Koffie, Robert M et al. (2011) Are tangles as toxic as they look? J Mol Neurosci 45:438-44
Hopson, Kristen Park; Truelove, Jessica; Chun, Jerold et al. (2011) S1P activates store-operated calcium entry via receptor- and non-receptor-mediated pathways in vascular smooth muscle cells. Am J Physiol Cell Physiol 300:C919-26
Kopeikina, Katherine J; Carlson, George A; Pitstick, Rose et al. (2011) Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimer's disease brain. Am J Pathol 179:2071-82
Greene, Sarah J; Killiany, Ronald J; Alzheimer's Disease Neuroimaging Initiative (2010) Subregions of the inferior parietal lobule are affected in the progression to Alzheimer's disease. Neurobiol Aging 31:1304-11

Showing the most recent 10 out of 21 publications