Understanding normal brain development and function and how it is altered by disease, injury, or environmental factors is one of the most exciting frontiers remaining in biomedical science today. New knowledge and tools acquired over the past decade offer hope for the development of new therapies for neurodevelopmental disorders, psychiatric illnesses, spinal cord injury, stroke, and neurodegenerative diseases. However, to effectively apply basic science knowledge to address these neural disorders requires the training of a new generation of neuroscientists. The goal of this training program is to provide five trainees in the first two years of Ph.D. training with a deep understanding of nervous system function and dysfunction at multiple levels of organization (molecular, cellular, circuit, behavior) and with the ability to apply diverse approaches (molecular/genetic, physiology, imaging) to understand how the nervous system develops, functions, and responds to injury or disease. This will be achieved by a program of formal course work and laboratory rotations with a highly interactive group of trainers whose expertise spans a broad range of neuroscience, in addition to active, continuous self-learning though participation in journal clubs, outside seminars, and other interactive forums. The program is aimed at equipping the trainees with the skills needed to identify and solve important problems throughout their careers as independent scientists.

Public Health Relevance

The training provided by this program will enable a new generation of neuroscientists to apply their knowledge of basic neuroscience mechanisms to develop therapies for neurodevelopmental disorders, psychiatric illnesses, spinal cord injury, stoke, and neurodegenerative disorders.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Institutional National Research Service Award (T32)
Project #
5T32NS067431-13
Application #
8085710
Study Section
Special Emphasis Panel (ZHD1-MRG-C (32))
Program Officer
Korn, Stephen J
Project Start
1999-09-01
Project End
2014-06-30
Budget Start
2011-07-01
Budget End
2012-06-30
Support Year
13
Fiscal Year
2011
Total Cost
$213,204
Indirect Cost
Name
Case Western Reserve University
Department
Neurosciences
Type
Schools of Medicine
DUNS #
077758407
City
Cleveland
State
OH
Country
United States
Zip Code
44106
Jay, Taylor R; Hirsch, Anna M; Broihier, Margaret L et al. (2017) Disease Progression-Dependent Effects of TREM2 Deficiency in a Mouse Model of Alzheimer's Disease. J Neurosci 37:637-647
Lindborg, Jane A; Mack, Matthias; Zigmond, Richard E (2017) Neutrophils Are Critical for Myelin Removal in a Peripheral Nerve Injury Model of Wallerian Degeneration. J Neurosci 37:10258-10277
Puzerey, Pavel A; Kodama, Nathan X; Galán, Roberto F (2016) Abnormal cell-intrinsic and network excitability in the neocortex of serotonin-deficient Pet-1 knockout mice. J Neurophysiol 115:813-25
Wyler, Steven C; Spencer, W Clay; Green, Noah H et al. (2016) Pet-1 Switches Transcriptional Targets Postnatally to Regulate Maturation of Serotonin Neuron Excitability. J Neurosci 36:1758-74
Jay, Taylor R; Miller, Crystal M; Cheng, Paul J et al. (2015) TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer's disease mouse models. J Exp Med 212:287-95
Skerrett, Rebecca; Pellegrino, Mateus P; Casali, Brad T et al. (2015) Combined Liver X Receptor/Peroxisome Proliferator-activated Receptor ? Agonist Treatment Reduces Amyloid ? Levels and Improves Behavior in Amyloid Precursor Protein/Presenilin 1 Mice. J Biol Chem 290:21591-602
DeFrancesco-Lisowitz, A; Lindborg, J A; Niemi, J P et al. (2015) The neuroimmunology of degeneration and regeneration in the peripheral nervous system. Neuroscience 302:174-203
Wyler, Steven C; Donovan, Lauren J; Yeager, Mia et al. (2015) Pet-1 Controls Tetrahydrobiopterin Pathway and Slc22a3 Transporter Genes in Serotonin Neurons. ACS Chem Neurosci 6:1198-205
Savage, Julie C; Jay, Taylor; Goduni, Elanda et al. (2015) Nuclear receptors license phagocytosis by trem2+ myeloid cells in mouse models of Alzheimer's disease. J Neurosci 35:6532-43
Puzerey, Pavel A; Decker, Michael J; Galán, Roberto F (2014) Elevated serotonergic signaling amplifies synaptic noise and facilitates the emergence of epileptiform network oscillations. J Neurophysiol 112:2357-73

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