Harrison School of Pharmacy
Faculty and Staff Directory
Unit: Drug Discovery and Development
Harrison School of Pharmacy
153 Pharmacy Research Building
Auburn, AL 36849
- B.A., Psychology - Auburn, 2002
- M.S., Experimental Psychology - Auburn, 2005
- Ph.D., Experimental Psychology - Auburn, 2007
2007-10: Postdoctoral Fellowship in Neuroscience and Neurology, University of Minnesota. Mentors: Karen Hsiao Ashe & James Cleary. Major Emphasis: Alzheimer’s Disease. Departments: Neuroscience, Neurology
2010-15: Assistant Professor, Behavioral Neuroscience - Department of Psychology; Member, Center for Neuroscience; Member, Center for Basic and Translational Stroke Research, West Virginia University.
Therapeutic Interventions for Alzheimer’s disease. Alzheimer’s disease (AD) affects one in every nine adults age 65 and older and is the sixth leading cause of death in the United States. As the average life expectancy increases, the incidence of AD is expected to increase dramatically. Meanwhile, pharmacologic treatments for AD have been ineffective at slowing or halting the disease. Therefore, it is imperative that alternative therapeutic targets be explored.
Over the course of Alzheimer’s disease, multiple biochemical pathways are perturbed, and a multiple-target approach is likely to be more effective than a single target approach. Using a variety of approaches, we identify therapeutic targets that may reduce the cognitive decline associated with AD. We are also examining whether already FDA-approved drugs can ameliorate memory deficits.
Neuronal Hyperexcitability. Alzheimer’s disease is a neurodegenerative disorder that targets connected neuronal networks. Effective regulation of activity in these neural networks is essential; over- or under- stimulation can erode synaptic regulation, leading to alterations in learning and memory, and more concerning, neurodegeneration throughout vulnerable networks. A particularly interesting phenomenon observed in the years preceding AD diagnosis, before neuronal death occurs, is a hyperactivity of the memory network. We use technically innovative approaches to examine alterations in the memory network early during the disease process.
Risk factors for AD. We examine how known risk factors, such as aging (the greatest known risk factor for AD), diabetes, and stroke, increase the likelihood of developing AD later in life. The goal is to not only understand why these factors increase the risk for AD but also how drug therapies may act differently in individuals comorbid for two or more diseases. Preclinical mouse models typically use mice exhibiting only one type of pathology (e.g., AD). Current models do not allow us to determine whether having multiple conditions, such as AD and diabetes, decrease the efficacy of therapeutics or increase in the side effects.
Intermittent Infection/Inflammation and Cognitive Aging. Role: Co-Principal Investigator. Agency: NIH/NIGMS U54GM104942 - Clinical and Translational Science Institute. Dates: 11/01/2014 – 05/30/2016.
Determining the Roles of Aging and Extrasynaptic NMDARs in Tau Pathology. Role: Principal Investigator. Agency: NIH/NIA R15AG045812. Dates: 07/15/2015 - 06/30/2018.
Comparison of Amyloid Beta Species. Principal Investigator: Miranda N. Reed. Agency: NIH T32 DA022616-02. Dates: 09/01/2007-09/01/2009.
Effects of Risk Factors on Tau-Mediated Memory Deficits. Role: Principal Investigator. Agency: NIRG-12-242187 - Alzheimer’s Association New Investigator Award. Dates: 11/01/2012 – 04/30/2015.
Increased Clearance of Extracellular Glutamate as a Treatment for Alzheimer’s Disease. Role: Principal Investigator. Agency: NIH/NIGMS U54GM104942 - Clinical and Translational Science Institute. Dates: 06/01/2013 – 11/30/2014.
Research Training Program in the Behavioral and Biomedical Sciences. Director: Albert Berrebi, PhD. Role: Steering Committee, BBS Scholarship, & Preceptor. Agency: NIH T32GM081741. Dates: 06/01/2014 - 05/30/2019.
(*indicates graduate students & ** indicates undergraduate students)
- Reed, M.N., Kotilinek, L.A., & Ashe, K.H. (2010). Effect size of Morris water maze deficits inTg2576 mice. Behavioural Brain Research, 212, 115-120.
- Hoover, B.R., Reed, M.N., Su, J., Kotilinek, K., Penrod, R.D., Pitstick, R., Carlson, G.A., Lanier, L.M., Yuan, L., Ashe, K.H., & Liao, D. (2010). Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration. Neuron, 68, 1-15.
- Reed, M.N., Hofmeister, J.J., Jungbauer, L., Welzel, A.T., Yu, C., Lesne, S., LaDu, M.J., Walsh, D.M., Ashe, K.H., & Cleary, J.P. (2011). Cognitive effects of cell-derived and synthetically-derived Aβ oligomers. Neurobiology of Aging, 32, 1784-94.
- Klyubin, I., Wang, Q., Reed, M.N., Irving, E.A., Upton, N., Hofmeister, J., Cleary, J.P., Anwyl, R., & Rowan, M.J. (2011). Protection against Abeta-mediated rapid disruption of synaptic plasticity and memory by Memantine. Neurobiology of Aging, 32, 614-23.
- *Petrone, A.B., Gatson, J.W., Simpkins, J.W., & Reed, M.N. (2014). Non-feminizing estrogens: a novel neuroprotective therapy. Molecular & Cellular Endocrinology, 389, 40-47.
- Reed, M.N., *Doll, D., Simpkins, J.W., & Barr, T. (2014). Aging & stroke: The human condition. Proceedings Nestle Purina Companion Animal Nutrition Summit: Nutrition for Life. March 27-29, 2014, Austin, Texas.
- **Povroznik, J.M., *Rudy, C.C., *Hunsberger, H.C., *Tosto, D.E., & Reed, M.N. (2014). Effects of an α5GABAA inverse agonist on MK-801-induced learning deficits in an incremental repeated acquisition task. Behavioural Pharmacology, 25, 331-335.
- *Hunsberger, H.C., *Rudy, C.C., *Weitzner, D.S., Zhang, C., *Tosto, D.E., **Knowlan, K., Xu, Y., & Reed, M.N. (2014). Effect size of memory deficits in mice with adult-onset P301L tau expression. Behavioural Brain Research, 6(272C), 181-195.
- *Petrone, A.B., *Rudy, C.C., Barr, T.L., Simpkins, J.W., & Reed, M.N. (2015). Neuroprotective effects of estrogen following neural injury. In: Estrogen effects on TBI: Mechanisms of neuroprotection and repair. Ed: K.A. Duncan. Elsevier Inc. Pgs. 91-111.
- Newland, M.C., Reed, M.N., & Rasmussen, E. (2015). A hypothesis about how early developmental methylmercury exposure disrupts behavior in adulthood. Behavioural Processes, 114, 41-51.
- *Hunsberger, H.C., *Rudy, C.C., Batten, S.R., Gerhardt, G.A., & Reed, M.N. (2015). P301L tau expression affects glutamate release and clearance in the hippocampal trisynaptic pathway. Journal of Neurochemistry, 32(2), 169-82.
- Liu, P., Reed, M.N., Kotilinek, L.A., Grant, M., Forster, C.L., Qiang, W., Shapiro, S.L., Reichl, J.H., Chiang, A., Jankowsky, J.L., Wilmot, C.M., Cleary, J.P., Zahs, K.R., & Ashe, K.H. (2015). Quaternary structure defines a large class of amyloid-β oligomers neutralized by sequestration. Cell Reports, 11, 1-12.
- *Weitzner, D.S., Engler-Chiurazzi, E.B., Kotilinek, L.A., Ashe, K.H., & Reed, M.N. (2015). Morris water maze test: Optimization for strain and testing environment. The Journal of Visualized Experiments (JoVE).
- *Rudy, C.C., *Hunsberger, H.C., *Weitzner, D.S., & Reed, M.N. (2014). The role of the tripartite glutamatergic synapse in the pathophysiology of Alzheimer's disease. Aging & Disease, 6(2), 131–148.
- Pan, J., Sun, J., Ding, L., Ruan, L., Reed, M.N., Yu, X., Klabni, J., Lin, D., Li, J., Chen, L., Zhang, C., Zhang, H., O'Donnell, J.M., & Xu, Y. (2014). Inhibition of phosphodiesterase 2 reverses impaired cognition and neuronal remodeling caused by chronic stress. Neurobiology of Aging, [Epub ahead of print].
- *Hunsberger, H.C., *Weitzner, D.S., *Rudy, C.C., **Hickman, J.E., **Libell, E.M., **Speer, R.R., Gerhardt, G.A., Reed, M.N. (2015). Riluzole rescues glutamate alterations, cognitive deficits, and tau pathology associated with P301L tau expression. Journal of Neurochemistry, [Epub ahead of print].