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Paula M. Keeney

Paula M. Keeney

Lab and Research Manager


Kontos Medical Sciences Building, Room 235
1217 East Marshall Street
Richmond, Virginia 23298

“The thing that got me interested in working with Dr. Bennett was the basic theory that mitochondria — the power houses in our cells — are what are causing a lot of the major problems with diseases like Parkinson’s. And that just was really interesting to me.”

Educational background

  • B.S., James Madison University
  • Curry School of Education, University of Virginia
  • Graduate School of Management and Technology, University of Maryland University College


Immersed in the study of mitochondria and their contribution to the development and progression of neurodegenerative diseases.   Current studies center on  investigating the roles of bioenergentics, mitochondrial genetics and cell signaling as they contribute to these diseases.

Recent professional achievements

  • Organized and executed the move of a large, active research unit from the University of Virginia to VCU
  • Currently assisting in the initiation of a program for the collection, storage and dispersal of post-mortem human brain samples at VCU
  • Learned, refined and taught the technique of laser capture microscopy (LCM) allowing the isolation of single neurons from post mortem brain; LCM and subsequent molecular biological analysis of LCM samples has allowed the lab to investigate the mitochondrial genetics of individual neurons free of surrounding tissues
  • Traveled to Austria for training on sensitive new equipment for measuring oxygen consumption at the cellular level
  • Isolation of mitochondria from human brain samples allowing analysis; results showed damage to a major protein group in Parkinson’s disease samples; this protein complex is a key component of the Electron Transport Chain that produces energy crucial to neuron function and survival

Recent publications

  • Thomas RR, Keeney PM, Bennett JP Jr. (2012) Impaired complex-I mitochondrial biogensis in Parkinson disease frontal cortex. J. Parkinsons Dis. 2012;2(1):67-76.
  • Keeney, PM and Bennett, JP, “ALS spinal neurons show varied and reduced mtDNA gene copy numbers and increased mtDNA gene deletions.”  Molecular Neurodegeneration, Vol. 5, Article No. 21; May 26, 2010.
  • Keeney PM, Dunham, LD, Quigley CK, et al.,  “Cybrid models of Parkinson’s disease show variable mitochondrial biogenesis and genotype-respiration relationships.”  Experimental Neurology, Vol. 220, Issue 2, pp. 374-382: Dec. 2009
  • Arthur CR, Morton SL, Dunham LD, et al.,  “Parkinson’s disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance.”  Molecular Neurodegeneration, Vol. 4, Article No. 37; Sept 23, 2009.
  • Keeney PM, Quigley CK, Dunham LD, et al.,  “Mitochondrial gene therapy augments mitochondrial physiology in a Parkinson’s disease cell model.”  Human Gene Therapy, Vol. 20, Issue 8, pp. 897-907; Aug 2009.
  • Borland MK, Trimmer PA, Rubenstein JD, et al.,  “Chronic low-dose rotenone reproduces Lewy neuritis found in early stages of Parkinson’s disease, reduces mitochondrial movement and slowly kills differentiated SH-SY5Y neural cells.”  Molecular Degeneration, Vol. 3, Article No. 21; Dec 29, 2008.

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