Patrick Bradshaw

Associate Professor

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• bradshawp@etsu.edu
• 423-439-4767
• VA 178/B135

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EDUCATION

B.S. in Bioengineering - University of Illinois-Urbana
Ph.D. in Biochemistry - The Ohio State University

RESEARCH/TEACHING INTERESTS

1. Mechanisms of mitochondrial dysfunction in aging and neurodegenerative diseases
2. RNAi screening using C. elegans nematodes to identify genes mediating aging-induced mitochondrial dysfunction
3. Metabolic therapies with select amino acids, ketone bodies, and citric acid cycle intermediates for the treatment of aging-associated disorders

PUBMED

Pubmed Link to Publications

SELECTED PUBLICATIONS

Delic, V., Brownlow, M., Joly-Amado, A., Zivkovic,  S., Noble, K., Phan, T., Ta, Y., Zhang, Y., Bell, S.D., Kurien, C., Reynes, C., Morgan, D., and Bradshaw, P.C. (2015) Calorie restriction does not restore brain mitochondrial function in P301L tau mice, but it does decrease mitochondrial F0F1-ATPase activity Molecular and Cellular Neuroscience 67:46-54.

ONeal-Moffitt, G., Delic, V., Bradshaw, P.C., and Olcese J. (2015) The role of membrane receptors in mediating the neuroprotective effects of melatonin in an APPswe/PS1 mouse model of Alzheimers disease Molecular Neurodegeneration 10:27.

Edwards, C., Copes, N., and Bradshaw, P.C. (2015) D--hydroxybutyrate: an anti-aging ketone body Oncotarget 6(6):3477-3478.

Edwards, C., Canfield, J., Copes, N., Rehan, M., Lipps, D., Brunquell, J., Westerheide, S.D., and Bradshaw, P.C. (2015) Mechanisms of amino acid-mediated lifespan extension in Caenorhabditis elegans. BMC Genetics 16:8.

Edwards, C., Canfield, J., Copes, N., Rehan, M., Lipps, D., and Bradshaw, P.C.  D-beta-hydroxybutyrate extends lifespan in C. elegans. (2014) Aging (Albany, NY) 6(8) 621-44.

Edwards, C., Copes, N., Canfield, J., Brito, A., and Bradshaw, P.C.(2013)Malate and fumarate extend lifespan in Caenorhabditis elegans. PLoS One 8(3):e58345.

Dragicevic, N., Delic, V., Cao, C., Copes, N., Lin, X., Mamcarz, M., Wang, L., Arendash, G.W., and Bradshaw, P.C.(2012)Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimers mice and cells. Neuropharmacol.  63(8) 1368-79.

Dragicevic, N., Smith, A., Lin, X., Yuan, F., Copes, N., Delic, V., Tan, J., Cao, C., Shytle, R.D., and Bradshaw, P.C.  (2011)Green tea epigallocatechin-3-gallate (EGCG) and other flavonoids reduce Alzheimers amyloid-induced mitochondrial dysfunction. J. Alzheimers Dis. 26(3):507-21.

Dragicevic, N., Copes, N., ONeal-Moffitt, G, Jin, J., Buzzeo, R., Mamcarz, M., Tan, J., Cao, C., Olcese, J.M. Arendash, G.W. and Bradshaw, P.C. (2011) Melatonin treatment restores mitochondrial function in Alzheimers mice: A mitochondrial protective role of melatonin membrane receptor signaling. J. Pineal. Res. 51:75-86.

DragicevicN., Mamcarz, M., Zhu, Y., Buzzeo, R., Tan, J., Arendash, G. A., and Bradshaw, P.C.(2010) Mitochondrial amyloid- levels are associated with the extent of mitochondrial dysfunction in different brain regions and the degree of cognitive impairment in Alzheimers transgenic mice. J. Alzheimers Dis. 20 Suppl 2, S535-50.