Predoctoral and postdoctoral students will receive comprehensive training in the Neurobiology and Neuropsychology of Aging through the combined efforts of a total of 17 mentors that include neurobiologists, neuropsychologists and neuroimagers at Boston University School of Medicine (N=12) and Massachusetts General Hospital, Harvard Medical School (N=5). Training will include research and didactics in (1) animal models of normal aging and age-related disease, (2) neuropsychology of aging and age-related neurologic disease, and (3) state-of-the art techniques in neuroimaging. Resources are founded on extensive research activity and grant support of the trainers that include several NIA funded program projects, two Alzheimer Disease Centers, and over 20 individual grants. With experience gained through active participation as one of the selected partners in the Carnegie Initiative for the Doctorate, a Roadmap grant to create one of the first Interdisciplinary Courses in Aging (Introduction to Interdisciplinary Systems Science: Dynamic Modeling), specific courses in the Foundations of Neuroimaging, and the Vesalius Program in Teaching in the Biomedical Sciences, this program provides a unique and progressive training in the neurobiology of aging. The areas of research represented among the training cadre include the neuropsychology and neurobiology (including neurogenetics) of Alzheimer's disease and Parkinson's disease, normal aging and cerebrovascular disease in non-human primate models, and studies of age-related changes at the cellular, synaptic ultrastructure and neuroimaging levels. All students will have a training experience with animal models (non-human primates and rodent) and humans encompassing (1) neuropsychological (2) structural and (3) imaging studies. The program includes, among other features, in-depth classroom instruction, methods in neuroscience with an emphasis on aging, hands-on laboratory research, the Vesalius course in biomedical teaching, and a course in interdisciplinary systems science and dynamic modeling.
| 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 |
| 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; Hyman, Bradley T; Spires-Jones, Tara L (2012) Soluble forms of tau are toxic in Alzheimer's disease. Transl Neurosci 3:223-233 |
| 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 |
| 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 |
| 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
