The Neuropathology Research Laboratory under the direction of Dr. DeArmond has performed a service function through a series Neuropathology Cores (NP Core) as well as an hypothesis testing function in studies of prion diseases since 1984 in collaboration with Stanley Prusiner and about equally as long with George Carlson. The NP Cores have contributed directly to about 100 prion disease-related publications in that time. This NP Core will perform a full range of neuropathological and immunohistochemical services including: perfusion of animals when needed; dissection of brain tissues as needed; snap freezing brain and other tissues as needed; standard neurohistological stains on formalin-fixed, paraffin-embedded tissue sections; histochemical stains on cryostat sections of muscle; plastic embedding and toluidine blue staining of thick sections of peripheral nerve; electron microscopy; and full autopsies as needed. The NP Core has also pioneered development of techniques to identify and quantify PrPC and PrPsc in tissue sections. The two standard techniques we use today are: the hydrolytic autoclaving method to eliminate PrPC and localize PrPsc in formalin-fixed, paraffin-embedded sections and the histoblot technique that can localize and quantify either PrPC or PrPsc in unfixed, frozen tissue sections. The NP Core continues to test new PrP antibodies by these two immunohistochemical techniques. This core also maintains a bank of paraffin-embedded and frozen tissues. The NP Core maintains a now massive data base of over 8000 animals for which either neuropathological or histoblot analysis has been performed. The NP Core helps Project Leaders interpret the neuropathological/immunohistochemical findings in the context of their hypotheses and questions, quantifies neuropathological and immunohistochemical results as needed, and prepares both black and white or color publication and notebook quality reproductions.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Program Projects (P01)
Project #
5P01NS041997-02
Application #
6642394
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
2002-08-01
Project End
2003-07-31
Budget Start
Budget End
Support Year
2
Fiscal Year
2002
Total Cost
Indirect Cost
Name
Mc Laughlin Research Institute
Department
Type
DUNS #
City
Great Falls
State
MT
Country
United States
Zip Code
59405
Chaverra, Marta; George, Lynn; Mergy, Marc et al. (2017) The familial dysautonomia disease gene IKBKAP is required in the developing and adult mouse central nervous system. Dis Model Mech 10:605-618
Daude, Nathalie; Lee, Inyoul; Kim, Taek-Kyun et al. (2016) A Common Phenotype Polymorphism in Mammalian Brains Defined by Concomitant Production of Prolactin and Growth Hormone. PLoS One 11:e0149410
Wegmann, Susanne; Maury, Eduardo A; Kirk, Molly J et al. (2015) Removing endogenous tau does not prevent tau propagation yet reduces its neurotoxicity. EMBO J 34:3028-41
Anderson, Sarah R; Lee, Inyoul; Ebeling, Christine et al. (2015) Disrupted SOX10 function causes spongiform neurodegeneration in gray tremor mice. Mamm Genome 26:80-93
Park, Laibaik; Koizumi, Kenzo; El Jamal, Sleiman et al. (2014) Age-dependent neurovascular dysfunction and damage in a mouse model of cerebral amyloid angiopathy. Stroke 45:1815-21
Lausted, Christopher; Lee, Inyoul; Zhou, Yong et al. (2014) Systems approach to neurodegenerative disease biomarker discovery. Annu Rev Pharmacol Toxicol 54:457-81
Stöhr, Jan; Condello, Carlo; Watts, Joel C et al. (2014) Distinct synthetic A? prion strains producing different amyloid deposits in bigenic mice. Proc Natl Acad Sci U S A 111:10329-34
Gunn, Teresa M; Carlson, George A (2013) RML prions act through Mahogunin and Attractin-independent pathways. Prion 7:267-71
Flores, Mauricio; Glusman, Gustavo; Brogaard, Kristin et al. (2013) P4 medicine: how systems medicine will transform the healthcare sector and society. Per Med 10:565-576
George, Lynn; Chaverra, Marta; Wolfe, Lindsey et al. (2013) Familial dysautonomia model reveals Ikbkap deletion causes apoptosis of Pax3+ progenitors and peripheral neurons. Proc Natl Acad Sci U S A 110:18698-703

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