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Faculty Detail    
Name RITA COWELL
 
Campus Address SC 843 Zip 0017
Phone  (205) 975-1208
E-mail  rcowell@uab.edu
Other websites
     

Education
Undergraduate  University of Illinois at Urbana-Champaign    1997  B.S. Honors Biology 
Graduate  University of Michigan    2002  Ph.D. Neuroscience 
Fellowship  University of Michigan    2006  Postdoctoral Fellowship 


Faculty Appointment(s)
Appointment Type Department Division Rank
Center  Alzheimer's Disease Center  Alzheimer's Disease Center Professor
Center  Comprehensive Neuroscience Center  Comprehensive Neuroscience Center Professor
Center  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Professor
Primary  Neurology Chair Office  Neurology Chair Office Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Genetics, Genomics and Bioinformatics 
Medical Scientist Training Program 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
1997 B.S. in Biology, University of Illinois, Urbana-Champaign 2002 Ph.D. in Neuroscience, University of Michigan, Ann Arbor 2002-6 Postdoctoral Fellow in Neurology, University of Michigan 2006-2014 Assistant Professor, Psychiatry, UAB 2014-2017 Associate Professor, Psychiatry, UAB 2015-2017 Co-Director, Neuroscience Graduate Program 2015-2017 Associate Director for Education and Outreach, Civitan International Research Center 2017-present Fellow and Chair of Neuroscience, Southern Research 2017-present Adjunct Associate Professor, Cell, Developmental, and Integrative Biology, UAB

Society Memberships
Organization Name Position Held Org Link
American Association for the Advancement of Science      
American College of Neuropsychopharmacology  Publications Committee   
Society for Neuroscience     



Research/Clinical Interest
Title
Cellular Vulnerability in Development and Aging: Using the Molecular Phenotype of Neurons to Elucidate Mechanisms of Disease and Identify Targets for Intervention
Description
Selective vulnerability of discrete neuronal populations gives rise to the diverse array of behavioral phenotypes characteristic of neurological and psychiatric disorders. In many disease contexts, scientists argue that this vulnerability arises from mitochondrial dysfunction or a high metabolic demand of the affected neurons or circuits. To better understand selective vulnerability in the brain, my laboratory has investigated the transcriptional, functional, and behavioral consequences of reductions in the expression of PGC-1alpha and its interacting factors, which mediate the expression of genes for mitochondrial biogenesis and function. During our studies, we found that certain sets of mitochondrial genes are regulated in parallel with synaptic and structural genes in a region and cell-selective manner in the CNS. Surprisingly, cell types like dopaminergic neurons of the substantia nigra and medium spiny neurons of the striatum, vulnerable in Parkinson Disease and Huntington Disease, respectively, are especially deficient in PGC-1alpha and associated transcriptional regulators. However, our recent studies suggest that we can promote neuroprotection and neuronal remodeling in Parkinson Disease models by manipulating these pathways. Currently funded projects involve a combination of mouse models of Parkinson Disease, frontotemporal dementia, and ALS and cre-lox technologies to manipulate and evaluate gene expression and function in cell-selective ways, with the overarching goal of identifying approaches to promote neuronal plasticity, metabolism, and survival in the context of disease. The laboratory is funded by the National Institutes of Health, the Michael J. Fox Foundation for Parkinson's Research, and the Meyer Foundation.

Selected Publications 
Publication PUBMEDID
McMeekin LJ, Fox SN, Boas SM, Cowell RM. (2021) Dysregulation of PGC-1-dependent Transcriptional Programs in Neurological and Developmental Disorders: Therapeutic Challenges and Opportunities. Cells. 10(2):352.  33572179 
McMeekin LJ, Li Y, Fox SN, Crossman DK, Day JJ, Li Y, Detloff PJ, Cowell RM. (2018) Cell-specific deletion of PGC-1 from medium spiny neurons causes transcriptional alterations and age-related motor impairment. J. Neurosci. 38:3273-3286.   29491012 
Gcwensa NZ, Russell DL, Cowell RM, Volpicelli-Daley LA. (2021) Molecular Mechanisms Underlying Synaptic and Axon Degeneration in Parkinson’s Disease. Front. Cell. Neurosci. 15:626128.  33737866 
McMeekin LJ, Bartley AF, Bohannon AS, Adlaf EW, van Groen T, Boas SM, Fox SN, Detloff PJ, Crossman DK, Overstreet-Wadiche LS, Hablitz JJ, Dobrunz LE, Cowell RM. (2020) A role for PGC-1a in transcription and excitability of neocortical and hippocampal excitatory neurons. Neuroscience 435:73-94.  32222555 
McMeekin LJ, Lucas EK, Meador-Woodruff JH, McCullumsmith RE, Hendrickson RC, Roberts RC, Gamble KL, Cowell RM. (2015) Cortical PGC-1alpha-dependent transcripts are reduced in postmortem tissue from patients with schizophrenia. Schizophrenia Bull. In press.   26683626 
Bartley AM, Lucas EK, Brady L, Li Q, Hablitz JJ, Cowell RM, Dobrunz LE. (2015) Interneuron transcriptional dysregulation causes frequency-dependent alterations in the balance of inhibition and excitation in hippocampus. J. Neurosci. 35:15276-90.   26586816 
Lucas EK, Reid CS, McMeekin LJ, Dougherty SE, Floyd CL, Cowell RM. (2015) Cerebellar transcriptional alterations with Purkinje cell dysfunction and loss in mice lacking PGC-1alpha. Front. Cell. Neurosci. 8:441.   25610371 
Lucas EK, Dougherty SE, McMeekin LJ, Reid CS, Dobrunz LE, West AB, Hablitz JJ, Cowell RM. (2014) PGC-1alpha provides a transcriptional framework for synchronous neurotransmitter release from parvalbumin-positive interneurons. J. Neurosci. 34(43):14375-87.   25339750 
Dougherty SE, Bartley AF, Lucas EK, Hablitz JJ, Dobrunz LE, Cowell RM. (2014) Mice lacking the transcriptional coactivator PGC-1alpha exhibit alterations in inhibitory synaptic transmission in the motor cortex. Neuroscience 271:137-48.  24769433 
Dougherty SE, Hollimon J, McMeekin LJ, Bohannon AS, West AB, Lesort M, Hablitz JJ, Cowell RM. (2014) Hyperactivity and cortical disinhibition in mice with restriction of mutant huntingtin expression to parvalbumin-positive cells. Neurobiol. Disease 62:160-71.  24121117 
Jiang Z, Rompala G, Zhang S, Cowell RM, Nakazawa K. (2013) Social isolation exacerbates schizophrenia-like phenotypes via oxidative stress in cortical interneurons. Biol. Psychiatry, 73:1024-34.   23348010 
Dougherty SE, Reeves JL, Lesort M, Detloff PJ, Cowell RM. (2013) Purkinje cell dysfunction and loss in a knock-in model of Huntington Disease. Exp. Neurol. 240:96-102.  23195593 
Lucas EK, Dougherty SE, McMeekin LJ, Trinh AT, Reid CS, Cowell RM. (2012) Developmental Alterations in Motor Coordination and Medium Spiny Neuron Markers in Mice Lacking PGC-1alpha. PLoS One 7(8):e42878.   22916173 
Dougherty SE, Reeves JL, Lucas EK, Gamble KL, Lesort M, Cowell RM. (2012) Disruption of Purkinje cell function prior to huntingtin accumulation and cell loss in an animal model of Huntington Disease. Exp. Neurol. 236(1):171-8.   22579526 
Moehle M, Webber P, Tse T, Sukar N, Standaert D, DeSilva TM, Cowell RM, West AB. (2012) LRRK2 inhibition attenuates microglial inflammatory responses. J. Neurosci. 32:1602-11.  22302802 
Ma D, Li S, Lucas EK, Cowell RM, Lin JD. (2010) Neuronal inactivation of PPARg Coactivator 1a (PGC-1a) protects mice from diet-induced obesity and leads to degenerative lesions. J. Biol. Chem. 285:39087-95.  20947495 
Lucas EK, Markwardt S, Gupta S, Meador-Woodruff JH, Lin JD, Overstreet-Wadiche L, Cowell RM. (2010) Parvalbumin deficiency and GABAergic dysfunction in mice lacking PGC-1a. J. Neurosci. 30:7227-35.   20505089 
Cowell RM, Talati P, Blake KR, Meador-Woodruff JH, Russell JW. (2009) Identification of novel targets for PGC-1a and histone deacetylase inhibitors in neuroblastoma cells. Biochem. Biophys. Res. Commun. 379:578-82.   19118529 
Cowell RM, Blake KR, Russell JW. (2007) Localization of the transcriptional coactivator PGC-1a to GABAergic neurons during maturation of the rat brain. J. Comp. Neurol. 502:1-18.
 
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Keywords
Transcription, Parkinson Disease, ALS, frontotemporal dementia, movement disorders, Neuroanatomy, Metabolism, Mitochondria, Neurobiology, Mouse models