Michael Sandstrom, Ph.D.
Health Professions Building 2179
About Dr. Sandstrom:
Dr. Sandstrom earned his doctorate in Neuroscience from Ohio State University in 1998 where he worked with a Parkinson’s disease animal model to explore age-dependent brain plasticity associated with the nigrostriatal dopamine system. During a subsequent postdoctoral fellowship with Dr. George Rebec at Indiana University in Bloomington he mastered techniques of single-unit neurophysiological recording and explored contributions of ascorbate to basal ganglia function. In his current position as an associate professor of psychology and neuroscience at Central Michigan University he continues research in deteriorative diseases of the brain, exploring neurophysiological mechanisms underlying behavioral disruptions in a transgenic mouse model of Huntington’s disease (HD). Dr. Sandstrom focuses research primarily on awake and freely moving animal models focused particularly on the physiological side of behavioral neuroscience. Specifically, experiments explore mechanisms that underlie plasticity and recovery of the mammalian brain following neuronal deterioration-induced deficits that disrupt behavior. While the behavioral deficits in movement and cognition are a hallmark of the psychological attributes, Dr. Sandstrom is far more focused on the underlying physiological mechanisms that generate disrupted neuronal activity, and in measuring these as presumed precursors to outward behavior expression. Currently, Dr. Sandstrom is processing how neuronal stem cells incorporate themselves into the network of the basal ganglia, and how these new neurons acquire activities that correlate with improved movement skills in animals modeling HD. He is utilizing optogenetics to find these newly transplanted neurons and record their activities at various stages following transplantation while simultaneously tracking behavior improvements. Other techniques include in-vivo microdialysis, single unit electrophysiology, iontophoresis, immunohistochemistry, local intracranial infusions, and sophisticated molecular and neurochemical analysis strategies.
Sandstrom, M.I., Steffes, S.K., Jayaprakash, N., Wolfram-Aduan, A., and Dunbar, G.L., Book Chapter: Early Dysfunction of Neural Transmission and Cognitive Processing, in Huntington's Disease, In Huntington's Disease - Core Concepts and Current Advances, Nagehan Ersoy Tunali Ed., (February 2012),ISBN:978-953-307-953-0, InTech, Open Source & available from: http://www.intechopen.com/books/huntington-s-disease-core-concepts-and-current-advances/early-dysfunction-of-neural-transmission-and-cognitive-processing-in-huntington-s-disease
- Dey N.D., Bombard M.C., Roland B.P., Davidson S., Lu M., Rossignol J., Sandstrom M.I., Skeel R.L., Lescaudron L., & Dunbar G.L., Genetically engineered mesenchymal stem cells reduce behavioral deficits in the YAC 128 mouse model of Huntington's disease. Behavioural Brain Research. (2010), 214(2), 193-200.
- Sandstrom, M.I., and Steffes, S., Constructing inexpensive, flexible, and versatile microdialysis probes in an undergraduate microdialysis research lab, Journal of Undergraduate Neuroscience Education (JUNE), (2008), Fall Quarter, 7(1), A33-A47.
- Dunbar, G.L., Sandstrom, M.I., Rossingnol, J., and Lescaudron, L., (2006) Neurotrophic enhancers as therapy for behavioral deficits in rodent models of Huntington's Disease: Use of gangliosides, substituted pyrimidines, and mesenchymal stem cells, Behavioral and Cognitive Neuroscience Reviews , 5(2), 63-79.
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