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The Ted Dawson Laboratory uses genetic, cell biological and biochemical approaches to explore the pathogenesis of Parkinson's disease (PD) and other neurologic disorders. We also investigate several discrete mechanisms involved in cell death, including the role of nitric oxide as an endogenous messenger, the function of poly (ADP-ribose) polymerase-1 and apoptosis inducing factor in cell death, and how endogenous cell survival mechanisms protect neurons from death.
The Calabresi Lab is located in the department of Neurology at the Johns Hopkins University School of Medicine. Our group investigates why remyelination occasionally fails following central nervous system demyelination in diseases like multiple sclerosis. Our primary focus is on discovering the role of t-cells in promoting or inhibiting myelination by the endogenous glial cells.
Five to 35 percent of spine fusionprocedures fail, even when using the gold standard treatment of grafting bone from the patient's own iliac crest. Fusion failure, otherwise known as pseudoarthrosis, is a major cause of failed back surgery syndrome (FBSS) and results in significant pain and disability, increasing the need for additional procedures and driving up health care costs. The ultimate goal of the Spinal Fusion Laboratory is to eliminate pseudoarthrosis by using animal models to study various strategies for improving spinal fusion outcomes, including delivery of various growth factors and biological agents; stem cell therapies and tissue engineering approaches.
We are exploring whether anodal tDCS when administered in combination with spelling, naming, or working memory therapy can improve language performance of PPA and MCI participants at least in the short term more than behavioral therapy alone. We are also investigating whether and how tDCS alters the neuropeptide signature in participants with PPA and MCI. We use proton magnetic resonance spectroscopy (1H-MRS) to monitor neuropeptide concentrations at the areas of stimulation. We hypothesize that tDCS will stabilize the decline of specific neuropeptides, but only in those areas of the brain where tDCS effectively results in more efficient gains in language compared to language therapy alone (with sham tDCS). Study results may help optimize future intervention in individuals with PPA and MCI by providing treatment alternatives in a neurodegenerative condition with no proven effective treatment. A better understanding of the therapeutic and neuromodulatory effects of tDCS in PPA and MCI will offer insight into ways of impeding neurodegeneration that may improve quality of life for individuals with PPA and MCI and may provide insights into the mechanisms of this treatment for augmenting therapy for stroke as well.
Improved acute stroke care means that more patients are surviving. Unfortunately, up to 60 percent of stroke survivors suffer disability in arm or leg use, and 30 percent need placement in a longer term care facility. Recovering motor skills after stroke is essential to rehabilitation and the restoration of a meaningful life. Therefore, there is an urgent need to develop innovative new approaches to rehabilitation. Most recovery from motor impairment after stroke occurs in the first month and is largely complete by three months. Improvement occurs independently of rehabilitative interventions (for example, physical and occupational therapy), which predominantly target function through compensatory strategies that do not constitute true recovery. Dr. Zeiler and his team are conducting research to uncover how to augment and prolong this critical window of time.
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