Linda C. Cork
Profile: http://med.stanford.edu/profiles/Linda_Cork/
Contact: Academic Appointments
Appointment
Organization
Professor
Member
|
Honors & Awards
Title
Organization
Date(s)
Distinguished Alumni
Texas A&M University
1991
Active Member
Institute of Medicine
1988
Councilor
American College of Veterinary Pathologists
1989-1992
Vice President
American College of Veterinary Pathologists
1997
President
American College of Veterinary Pathologists
1996
7 honors and awards: view full list
Administrative Appointments
Title
Organization
Start Year
End Year
Chair
Stanford University School of Medicine - Comparative Medicine
2000
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Professional Education
Degree
Awarding Institution
Field of Study
Year of Graduation
D.V.M.
Texas A & M University
Veterinary Medicine
1970
Ph.D.
Washington State University
Experimental Pathology
1974
Web Site Links
Research/Lab website:
Department of Comparative Medicine
Research Interests
Animal models offer a unique opportunity to study the pathogenesis of neurologic diseases afflicting both humans and animals. For example, non-human primates develop many of the same cognitive deficits and neuropathologic changes as occur in humans. Inherited diseases in dogs reliably replicate many hereditary diseases in humans. We can learn much by studying the temporal and spatial evolution of the lesions in the nervous system in spontaneously occurring or induced diseases in animals.The rapid development of the dog genome map brings an important benefit to the study of inherited canine diseases. Comparative gene mapping among human, murine, and canine genomes have the potential to rapidly identify mutations that underlie various disease syndromes. My research focuses on the identification and characterization of animal models of human diseases. These animal models may occur in non-human primates, dogs, cats, goats, mice in which mutations have been induced, or in other less common laboratory species such as bears. By using these diverse species we can ask how the nervous system lesions are related to functional deficits? What is the biological significance of the lesions? How do the lesions begin? How do they evolve? What is the function of the cells early in disease when therapeutic intervention would be most advantageous? By evaluating the pathology and physiologic function or behavior in animals, we can begin to design rational interventional strategies to prevent, treat, or to delay the onset of neurodegenerative diseases.
Publications
- Green SL, Westendorf JM, Jaffe H, Pant HC, Cork LC, Ostrander EA, Vignaux F, Ferrell JE "Allelic variants of the canine heavy neurofilament (NFH) subunit and extensive phosphorylation in dogs with motor neuron disease." J Comp Pathol 2005; 132: 1: 33-50 More »
- Tolwani R, Hagan C, Runstadler J, Lyons H, Green S, Bouley D, Rodriguez L, Schendel S, Moseley M, Daunt D, Otto G, Cork L "Magnetic resonance imaging and surgical repair of cleft palate in a four-week-old canine (Canis familiaris): an animal model for cleft palate repair." Contemp Top Lab Anim Sci 2004; 43: 6: 17-21; quiz 58 More »
- Green SL, Tolwani RJ, Varma S, Quignon P, Galibert F, Cork LC "Structure, chromosomal location, and analysis of the canine Cu/Zn superoxide dismutase (SOD1) gene." J Hered 2002 Mar-Apr; 93: 2: 119-24 More »
- Green SL, Bouley DM, Pinter MJ, Cork LC, Vatassery GT "Canine motor neuron disease: clinicopathologic features and selected indicators of oxidative stress." J Vet Intern Med 2001 Mar-Apr; 15: 2: 112-9 More »
- Balice-Gordon RJ, Smith DB, Goldman J, Cork LC, Shirley A, Cope TC, Pinter MJ "Functional motor unit failure precedes neuromuscular degeneration in canine motor neuron disease." Ann Neurol 2000; 47: 5: 596-605 More »
11 publications: view full list
