PO Box 9229
BMRF Room 105
- Petrone AB, Gatson JW, Simpkins JW, Reed MN. Non-feminizing estrogens: A novel neuroprotective therapy. Mol Cell Endocrinol (2013 Jan 11) [Epub ahead of print]
- Li W, Huang R, Shetty RA, Thangthaeng N, Liu R, Chen Z, Sumien N, Rutledge M, Dillon GH, Yuan F, Forster MJ, Simpkins JW, Yang SH. Transient focal cerebral ischemia induces long-term cognitive function deficit in an experimental ischemic stroke model. Neurobiol Dis (2013 Nov) 59:18-25.
- Harrison DE, Strong R, Allison DB, Ames BN, Astle CM, Atamna H, Fernandez E, Flurkey K, Javors MA, Nadon NL, Nelson JF, Pletcher S, Simpkins JW, Smith D, Wilkinson JE, Miller RA. Acarbose, 17-α-estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males. Aging Cell (2013 Oct 26) [Epub ahead of print]
- Phillips NR, Simpkins JW, Roby RK. Mitochondrial DNA deletions in Alzheimer's brains: A review. Alzheimers Dement (2013 Jul 11) [Epub ahead of print]
- Singh M, Simpkins JW, Bimonte-Nelson HA, Brinton RD. Window of opportunity for estrogen and progestin intervention in brain aging and Alzheimer's disease. Brain Res (2013 Jun 13) 1514:1-2.
- Richardson TE, Kelly HN, Yu AE, Simpkins JW. Therapeutic strategies in Friedreich's ataxia. Brain Res (2013 Jun 13) 1514:91-7.
- Lincoln KM, Gonzalez P, Richardson TE, Julovich DA, Saunders R, Simpkins JW, Green KN. A potent antioxidant small molecule aimed at targeting metal-based oxidative stress in neurodegenerative disorders. Chem Commun (Camb) (2013 Apr 4) 49(26):2712-4.
- Li W, Winters A, Poteet E, Ryou MG, Lin S, Hao S, Wu Z, Yuan F, Hatanpaa KJ, Simpkins JW, Yang SH. Involvement of estrogen receptor Β5 in the progression of glioma. Brain Res (2013 Mar 29) 1503:97-107.
- Poteet R, Choudhury GR, Winters A, Li W, Ryou MG, Liu R, Tang L, Ghorpade A, Wen Y, Yuan F, Keir ST, Yan H, Bigner DD, Simpkins JW, Yang SH. Reversing the Warburg effect as a treatment of glioblastoma. J Biol Chem (2013 Mar 29) 288(13):9153-64.
- Simpkins JW, Richardson TE, Yi KD, Perez E, Covey DF. Neuroprotection with non-feminizing estrogen analogues: an overlooked possible therapeutic strategy. Horm Behav (2013 Feb) 63(2):278-83.
Our lab studies the causes and potential treatment for Alzheimer’s disease (AD) and stroke in animal models and in human subjects. We are trying to understand the cause of brain damage from AD stroke and to develop treatments based on our understanding of causes. We use rats to induce stroke damage and a variety of techniques, including molecular biology, behavioral assessment and drug interventions to determine the causes and potential treatment for stroke damage. Our work also involves the use of transgenic mouse models, primarily for modeling AD. West Virginia has one of the highest incidences of stroke in the nation and currently therapies to limit stoke damage are limited. Our lab therefore is searching for novel treatments that can limit the damage and/or improve recovery from stroke.
Dana Foundation Blog: Dr. Simpkins on Stroke - http://danablog.org/2014/05/29/james-simpkins-on-stroke/
Center for Basic & Translational Stroke Research
- We assess the role of mitochondria in stroke propensity and stroke damage. These studies are aims at identifying the mechanism by which mitochondrial dysfunction contributes to stroke damage and the possibility of targeting drugs to these mitochondrial defects as a therapy for prevention/acute treatment of stroke.
- Assessment of vaious classes of drugs on neuroprotection in stroke and AD. We have a drug discovery program that attempts to discover novel compounds with efficacy in stroke and AD. One such class of compounds we have termed non-feminizing estrogens.
Structure and stroke protective effects of a non-feminizing estrogen (ZYC3)
- We assess the effects of beta amyloid on mitochondrial function to determine how this neurotoxic peptide causes loss of synapses and neurons in the brain.
Short-term treatment with beta amyloid (Abeta) causes a profound decline in mitochondrial function in promary neuronal cultures.