Dr. Jeffrey A. Rumbaugh received his Ph.D. in biochemistry and his medical degree from the University of Rochester, followed by an internship in internal medicine at The Johns Hopkins Bayview Medical Center. He completed his residency in neurology at The Johns Hopkins Hospital.

Now an Assistant Professor of Neurology, Dr. Rumbaugh specializes in infectious and immunological/inflammatory diseases which affect the nervous system. Examples include the West Nile virus and other viral encephalitides, Creutzfeld Jakob Disease and other prion diseases (human variants of mad cow disease), neurological complications of HIV/AIDS, central nervous system Lyme disease, multiple sclerosis, neurosarcoidosis, and central nervous system lupus and other CNS vasculitides.

Dr. Rumbaugh’s research interests focus on exploring the molecular mechanisms and interactions of human and viral factors as they relate to the development of neurodegeneration in patients with HIV dementia. All forms of dementia are caused by degeneration of neurons, but the reasons that the neurons degenerate are often not well understood. HIV dementia occurs without the virus actually infecting the neurons themselves. Neuronal damage must therefore occur by indirect means. For example, in response to viral infections in the brain, the normal functions of many human proteins are altered. Some of these alterations are detrimental to neuronal function, while others may be beneficial. An understanding of this delicate balance is essential to develop new modes of treatment, which optimize the beneficial functions and minimize the detrimental ones. An HIV protein, called Tat, and a family of human proteins, called matrix metalloproteinases (MMPs) are both involved in causing HIV dementia, and MMPs are involved in other forms of dementia as well. The possibility that these proteinases may interact with the viral pathogens themselves to either enhance or curtail neuropathogenesis remains critically unexplored. Dr. Rumbaugh's work demonstrates, for the first time, that human MMPs can interact with Tat and other viral proteins. Surprisingly, this interaction can actually be protective of brain function. These results suggest that MMPs may serve a previously unrecognized role as a human defense mechanism against infection, and may have both protective and deleterious effects in other forms of dementia. Dr. Rumbaugh's hope and expectation is that this basic research will not only advance clinical medicine through its therapeutic implications for many of the neurological complications of HIV disease but may have implications for understanding the pathophysiology of other viral encephalitides and other dementias as well.

Dr. Rumbaugh sees patients at The Johns Hopkins Outpatient Center in Baltimore on Mondays.

Certifications:

• American Board of Psychology and Neurology