Lyme disease is a major emerging infection in the United States, and has become a significant health issue in terms of public awareness, health care costs, and medical practice standards. Neurologic involvement is now recognized as the major morbidity of Lyme disease, but has not been studied in a systematic fashion. This Program Project has assembled an interdisciplinary team of investigators to study neurologic Lyme disease. They will utilize the clinical and laboratory resources of the Lyme Disease Center at Stony Brook. All components of this Program Project are linked by shared methodologies, conceptual frameworks, and common Cores. The three Clinical Projects will provide materials for the Pathogenesis Project: Project 1 will look at the role of host factors (the T cell response) and organism factors (neurotropism, antigenic variation). Project 2 will determine the frequency, correlates, and outcome of central nervous system invasion in early Lyme disease. Project 3 will characterize the neurobehavioral syndromes of chronic Lyme disease. Project 4 will study neurologic Lyme disease in children. The supporting Cores are: A) an Administrative Center Core; B) a Data Management Core; C) a Central Laboratory Core; D) a Neuropsychology Core. The primary scientific goals of this Program Project are 1) to identify and characterize prospectively the neurologic, neuropsychologic, and psychosocial manifestations of Lyme disease in children and adults; and 2) to identify pathogenetic mechanisms involved in neurologic Lyme disease. The secondary goals are 3) to characterize associated cerebrospinal fluid changes; and 4) to identify risk factors for poor outcome. This Program Project will support a structured interdisciplinary effort to study the neurologic aspects of Lyme disease. It will provide information to guide development of rational and cost-effective public health policy for this important infection.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Program Projects (P01)
Project #
5P01NS034092-05
Application #
6393711
Study Section
Special Emphasis Panel (ZNS1-SRB-H (J1))
Program Officer
Kerza-Kwiatecki, a P
Project Start
1997-04-01
Project End
2003-03-31
Budget Start
2001-04-01
Budget End
2003-03-31
Support Year
5
Fiscal Year
2001
Total Cost
$1,081,579
Indirect Cost
Name
State University New York Stony Brook
Department
Neurology
Type
Schools of Medicine
DUNS #
804878247
City
Stony Brook
State
NY
Country
United States
Zip Code
11794
Gilhar, A; Ullmann, Y; Karry, R et al. (2004) Ageing of human epidermis: the role of apoptosis, Fas and telomerase. Br J Dermatol 150:56-63
Fikrig, Erol; Coyle, Patricia K; Schutzer, Steven E et al. (2004) Preferential presence of decorin-binding protein B (BBA25) and BBA50 antibodies in cerebrospinal fluid of patients with neurologic Lyme disease. J Clin Microbiol 42:1243-6
Kalish, Richard S; Wood, Jonathan A; Golde, William et al. (2003) Human T lymphocyte response to Borrelia burgdorferi infection: no correlation between human leukocyte function antigen type 1 peptide response and clinical status. J Infect Dis 187:102-8
Gilhar, Amos; Landau, Marina; Assy, Bedia et al. (2002) Mediation of alopecia areata by cooperation between CD4+ and CD8+ T lymphocytes: transfer to human scalp explants on Prkdc(scid) mice. Arch Dermatol 138:916-22
Kumaran, D; Eswaramoorthy, S; Luft, B J et al. (2001) Crystal structure of outer surface protein C (OspC) from the Lyme disease spirochete, Borrelia burgdorferi. EMBO J 20:971-8
Schutzer, S E; Coyle, P K; Chen, D (2001) The role of the allergist in Lyme disease. Allergy Asthma Proc 22:29-31
Gilhar, A; Landau, M; Assy, B et al. (2001) Melanocyte-associated T cell epitopes can function as autoantigens for transfer of alopecia areata to human scalp explants on Prkdc(scid) mice. J Invest Dermatol 117:1357-62
Kalish, R S (2000) Pemphigus vulgaris: the other half of the story. J Clin Invest 106:1433-5
Schutzer, S E; Coyle, P K; Reid, P et al. (1999) Borrelia burgdorferi-specific immune complexes in acute Lyme disease. JAMA 282:1942-6
Gilhar, A; Shalaginov, R; Assy, B et al. (1999) Alopecia areata is a T-lymphocyte mediated autoimmune disease: lesional human T-lymphocytes transfer alopecia areata to human skin grafts on SCID mice. J Investig Dermatol Symp Proc 4:207-10

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