Linda C. Cork
Academic Appointments
- Professor, Comparative Medicine
- Member, Bio-X
Contact Information
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Academic Offices
Administrative Contact Janine Owens Administrative Assistant Email Tel Work 650 498-5080
Professional Snapshot
Administrative Appointments
- Chair, Stanford University School of Medicine - Comparative Medicine (2000 - present)
Honors and Awards
- 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)
Professional Education
| D.V.M.: | Texas A & M University, Veterinary Medicine (1970) |
| Ph.D.: | Washington State University, Experimental Pathology (1974) |
Postdoctoral Advisees
Graduate & Fellowship Program Affiliations
Web Site Links
Scientific Focus
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
- Allelic variants of the canine heavy neurofilament (NFH) subunit and extensive phosphorylation in dogs with motor neuron disease. J Comp Pathol. 2005; (1): 33-50
- 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; (6): 17-21; quiz 58
- Structure, chromosomal location, and analysis of the canine Cu/Zn superoxide dismutase (SOD1) gene. J Hered. 2002 Mar-Apr; (2): 119-24
- Canine motor neuron disease: clinicopathologic features and selected indicators of oxidative stress. J Vet Intern Med. 2001 Mar-Apr; (2): 112-9
- Functional motor unit failure precedes neuromuscular degeneration in canine motor neuron disease. Ann Neurol. 2000; (5): 596-605
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