McLaughlin Institute

George A. Carlson, PhD

Director and Professor

george carlson

Laboratory Members

Postdoctoral Fellows
Brenda Canine, Ph.D.
Andrea Grindeland, DVM

Administrative/Senior Research Assistant
Jill O’Moore

Senior Research Assistant
Rose Pitstick

Research Assistant
None at this time



University of Pennsylvania, AB, Biochemistry, 1969

Tufts University, PhD, Physiology, 1976 



1969-1970  Instructor of Biology. Berkshire School, Sheffield, MA

1973-1974  Lecturer in Physiology. Tufts-Boston School of Occupational Therapy, Boston, MA

1970-1975 Predoctoral Research Fellow. Dr. G. Terres, Tufts University School of Medicine, Boston, MA

1975-1977  Leukemia Society Postdoctoral Fellow. Dr. T.G. Wegmann, Department of Immunology, University of Alberta, Edmonton, Alberta, Canada (Immunogenetics)

1977-1980  Assistant Professor of Immunology. University of Alberta, Edmonton, Alberta, Canada

1980-1985  Associate Staff Scientist. The Jackson Laboratory, Bar Harbor, ME

1985-1988  Staff Scientist (Associate Professor). The Jackson Laboratory, Bar Harbor, ME

1988-2008  Adjunct Professor of Microbiology. Montana State University, Bozeman, MT

2008-present  Adjunct Professor of Cell Biology and Neuroscience. Montana State University, Bozeman, MT

1993-present  Adjunct Professor of Biological Sciences/Pharm. Sci. University of Montana, Missoula, MT

1993-1997  Advisor/Consultant. Millennium Pharmaceuticals, Inc., Cambridge, MA

1988-present  Director and Professor. McLaughlin Research Institute, Great Falls, MT


Major Areas of Research

Identification of early biomarkers for neurodegenerative disease detection.

Identification of common pathways involved in neurodegenerative diseases.


Description of Research

The underlying theme of Dr. Carlson’s research is the application of formal and molecular mouse genetics to advance the understanding of susceptibility to neurodegenerative diseases. George is now applying his expertise in mouse genetics to a systems analysis of prion disease in collaboration with Dr. Lee Hood at the Institute for Systems Biology in Seattle, Washington. Dr. Carlson and his colleagues also developed what may be the first genetically tractable in vitro model for prion disease by successfully infecting CNS stem cell containing neurosphere cultures. He is now using neurosphere cultures to model biochemical events in mouse models for frontotemporal dementia and other prion-like neurodegenerative disorders, several of which he was involved in creating.


Current Publications

Tara Leigh Spires-Jones, Leora M Fox, Anete Rozkalne, Rose Pitstick, George A. Carlson, Aleksey G. Kazantsev. Inhibition of sirtuin 2 with sulfobenzoic acid derivative AK1 is non-toxic and potentially neuroprotective in a mouse model of frontotemporal dementia. Frontiers in Experimental Pharmacology and Drug Discovery. In Press. PMID: 22416232

De Calignon A, Polydoro M, Suarez-Calvert M, William C, Adamowicz DH, Kopeikina KJ, Pitstick R, Sahara N, Ashe KH, Carlson GA, Spires-Jones TL, Hyman BT. Propagation of tau pathology in a model of early Alzheimer’s disease. Neuron. 2012 Feb 23; 73(4): 685-697. PMID: 22365544

Westaway D, Genovesi S, Daude N, Brown R, Lau A, Lee I, Mays CE, Coomaraswamy J, Canine B, Pitstick R, Herbst A, Yang J, Ko KWS, Schmitt-Ulms G, DeArmond S, McKenzie D, Hood L, Carlson GA. Down-regulation of Shadoo in prion infections traces a pre-clinical event inversely related to PrPSc accumulation. PloS Pathogens. 2011 Nov; 7(11):1-18. PMID: 22114562

Kopeikina KJ, Carlson GA, Pitstick R, Ludvigson AE, Luebke JI, Koffie RM, Frosch MP, Hyman BT, Spires-Jones TL. Tau Accumulation Causes Mitochondrial Distribution Deficits in Neurons in a Mouse Model of Tauopathy and in Human AD Brain.Am J Pathol. 2011 Oct; 179(4):2071-2082 PMID: 21854751

Lan X, Kiyota T, Hanamsagar R, Huang Y, Andrews S, Peng H, Zheng JC, Swindells S, Carlson GA, Ikezu T. The Effect of HIV Protease Inhibitors on Amyloid-β Peptide Degradation and Synthesis in Human Cells and Alzheimer’s Disease Animal Model.J Neuroimmune Pharmacol. 2011 Aug 9. [Epub ahead of print] PMID: 21826404

Fox LM, William CM, Adamowicz DH, Pitstick R, Carlson GA, Spires-Jones TL, Hyman BT. Soluble tau species, not neurofibrillary aggregates, disrupt neural system integration in a tau transgenic model.J Neuropathol Exp Neurol. 2011 Jul;70(7):588-95. PMID: 21666499

Park L, Wang G, Zhou P, Zhou J, Pitstick R, Previti M, Younkin L, Younkin S, Van Nostrand W, Cho S, Anrather J, Carlson G, Iadecola C. Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-beta. Proc Natl Acad Sci. (USA) 2011, 108(12): 5063-68. PMID: 21383152

Hnasko R, Serban AV, Carlson G, Prusiner SB, Stanker LH. Generation of antisera to purified prions in lipid rafts.  Prion. 2010 4(2): 94-104  Erratum to:  Generation of antisera to purified prions in lipid rafts. Prion. 2011 Jul 1;5(3). ). PMID; 21844667

Hoover B, Reed M, Su J, Penrod R, Kotilinek L, Gtant M, Pitstick R, Carlson GA, Lanier L, Yuan L, Ashe K, Liao D.  Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration.  Neuron.  2010, 68:1067-1081. PMID: 21172610

The Prion Disease Database (PDDB) is a public database that supports the prion disease research community by collecting, integrating, and presenting data from public sources and collaborating laboratories. The PDDB was originally created by the Institute for Systems Biology and the McLaughlin Research Institute, which have researched prion disease using a systems biology approach.

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