The goal of this Training Program is to prepare promising graduate students and postdoctoral fellows for successful careers in the neurobiology of aging. We will provide broad-based training in modern concepts in the neurobiology of aging with an emphasis on cellular and molecular mechanisms underlying aging processes and possible therapeutic interventions. The unifying focus of the training faculty is our interest in understanding both normal and pathological mechanisms by which the nervous system responds to changes that occur with age and emerging concepts in therapeutic intervention. This Training Program provides the formal framework for faculty in different departments, who share a common interest in the molecular- cellular basis of brain aging and translational research, to provide in-depth training in aging. The emphasis of the Training Faculty complement each other: some focus on processes that occur in the brain during normal aging, others emphasize the neuropathological processes of diseases and injuries that predominate in the aging brain, and there is a combined interest in applying this knowledge to treating neural disorders of aging. Thus, trainees will learn from faculty who utilize a broad spectrum of state-of-the-art methodological approaches to probe critical questions in aging research. Our successes attest to our abilityto identify, attract, train and place promising young investigators in the area of the neurobiology of aging. Now more than ever before, we are particularly qualified to train graduate students and postdoctoral fellows. The national need for training new investigators in the area of aging is clear due to our changing demography and the increasing average lifespan. Normal aging or pathology of the nervous system underlies much age-associated morbidity. Only if we better understand the basic mechanisms that regulate the aging of the brain and apply this to the treatment ofthe elderly, can we hope to improve the qualityof life during the latter half ofthe lifespan. Our ability to attract and train graduate students and postdoctoral fellows to meet the challenges in the area of the neurobiology of aging will be greatly enhanced by this Training Program.
This Program will train the next generation of scientists to carryout research on the neurobilogy of aging. Dramatic improvements in the treatment of age-related illnesses such as Alzheimer's disease, Parkinson's disease, stroke, epilepsy and others are need for the aging world population. Only through training of such research areas can we hope to make strides in new treatments for illnesses that cost us billions.
|Luo, Yi; Wu, Tingting; Broster, Lucas S et al. (2014) The temporal course of the influence of anxiety on fairness considerations. Psychophysiology 51:834-42|
|Fuqua, Joshua L; Littrell, Ofelia M; Lundblad, Martin et al. (2014) Dynamic changes in dopamine neuron function after DNSP-11 treatment: effects in vivo and increased ERK 1/2 phosphorylation in vitro. Peptides 54:1-8|
|Miller, Erin M; Pomerleau, Francois; Huettl, Peter et al. (2014) Aberrant glutamate signaling in the prefrontal cortex and striatum of the spontaneously hypertensive rat model of attention-deficit/hyperactivity disorder. Psychopharmacology (Berl) 231:3019-29|
|Stephens, Michelle L; Williamson, Anne; Deel, Megan E et al. (2014) Tonic glutamate in CA1 of aging rats correlates with phasic glutamate dysregulation during seizure. Epilepsia 55:1817-25|
|Latimer, Caitlin S; Brewer, Lawrence D; Searcy, James L et al. (2014) Vitamin D prevents cognitive decline and enhances hippocampal synaptic function in aging rats. Proc Natl Acad Sci U S A 111:E4359-66|
|Littrell, Ofelia M; Granholm, Ann-Charlotte; Gerhardt, Greg A et al. (2013) Glial cell-line derived neurotrophic factor (GDNF) replacement attenuates motor impairments and nigrostriatal dopamine deficits in 12-month-old mice with a partial deletion of GDNF. Pharmacol Biochem Behav 104:10-9|
|Littrell, O M; Fuqua, J L; Richardson, A D et al. (2013) A synthetic five amino acid propeptide increases dopamine neuron differentiation and neurochemical function. Neuropeptides 47:43-9|
|van Bregt, Daniel R; Thomas, Theresa Currier; Hinzman, Jason M et al. (2012) Substantia nigra vulnerability after a single moderate diffuse brain injury in the rat. Exp Neurol 234:8-19|
|Thomas, Theresa Currier; Hinzman, Jason M; Gerhardt, Greg A et al. (2012) Hypersensitive glutamate signaling correlates with the development of late-onset behavioral morbidity in diffuse brain-injured circuitry. J Neurotrauma 29:187-200|
|Sauerbeck, Andrew; Hunter, Randy; Bing, Guoying et al. (2012) Traumatic brain injury and trichloroethylene exposure interact and produce functional, histological, and mitochondrial deficits. Exp Neurol 234:85-94|
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