Danielle S. Goulding

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Overproduction of proinflammatory cytokines in the CNS has been implicated as a key contributor to pathophysiology progression in Alzheimer's disease (AD), and extensive studies with animal models have shown that selective suppression of excessive glial proinflammatory cytokines can improve neurologic outcomes. The prior art, therefore, raises the logical(More)
Adam D. Bachstetter,1 Rachel K. Rowe,2,3 Machi Kaneko,1 Danielle Goulding,1 Jonathan Lifshitz,4,5,6 and Linda J. Van Eldik1,2,3 1Sanders-Brown Center on Aging, 2Department of Anatomy and Neurobiology, and 3Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536, 4Barrow Neurological Institute at Phoenix Children’s(More)
Neuropathology after traumatic brain injury (TBI) is the result of both the immediate impact injury and secondary injury mechanisms. Unresolved post-traumatic glial activation is a secondary injury mechanism that contributes to a chronic state of neuroinflammation in both animal models of TBI and human head injury patients. We recently demonstrated, using(More)
Evidence from clinical studies and preclinical animal models suggests that proinflammatory cytokine overproduction is a potential driving force for pathology progression in traumatic brain injury (TBI). This raises the possibility that selective targeting of the overactive cytokine response, a component of the neuroinflammation that contributes to neuronal(More)
A prevailing neuroinflammation hypothesis is that increased production of proinflammatory cytokines contributes to progressive neuropathology, secondary to the primary damage caused by a traumatic brain injury (TBI). In support of the hypothesis, post-injury interventions that inhibit the proinflammatory cytokine surge can attenuate the progressive(More)
The calcium/calmodulin-dependent protein kinase II (CaMKII) is abundant in the brain, where it makes important contributions to synaptic organization and homeostasis, including playing an essential role in synaptic plasticity and memory. Four genes encode isoforms of CaMKII (α, β, δ, γ), with CaMKIIα and CaMKIIβ highly expressed in the brain. Decades of(More)
Adam D. Bachstetter,1 Christopher M. Norris,1,2 Pradoldej Sompol,1 Donna M. Wilcock,1,3 Danielle Goulding,1 Janna H. Neltner,1,4 Daret St. Clair,1,5,7 D. Martin Watterson,8 and Linda J. Van Eldik1,6 1Sanders-Brown Center on Aging, Departments of 2Molecular and Biomedical Pharmacology, 3Physiology, 4Pathology, 5Toxicology, and 6Anatomy and Neurobiology, and(More)
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