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Previous Article | Next Article
The Journal of Neuroscience, February 1, 1999, 19(3):928-939
Identification of Microglial Signal Transduction Pathways Mediating a Neurotoxic Response to Amyloidogenic Fragments of
-Amyloid and Prion Proteins
Colin K. Combs, Derrick E. Johnson, Steve B. Cannady, Timothy M. Lehman, and Gary E. Landreth Alzheimer Research Laboratory, Departments of Neurology and Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4928
Microglial interaction with amyloid fibrils in the brains of Alzheimer's and prion disease patients results in the inflammatory activation of these cells. We observed that primary microglial cultures and the THP-1 monocytic cell line are stimulated by fibrillar
-amyloid and prion peptides to activate identical tyrosine kinase-dependent inflammatory signal transduction cascades. The tyrosine kinases Lyn and Syk are activated by the fibrillar peptides and initiate a signaling cascade resulting in a transient release of intracellular calcium that results in the activation of classical PKC and the recently described calcium-sensitive tyrosine kinase PYK2. Activation of the MAP kinases ERK1 and ERK2 follows as a subsequent downstream signaling event. We demonstrate that PYK2 is positioned downstream of Lyn, Syk, and PKC. PKC is a necessary intermediate required for ERK activation. Importantly, the signaling response elicited by
Key words: Alzheimer's disease;
Copyright © 1999 Society for Neuroscience 0270-6474/99/193928-12$05.00/0
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