Dr. Prineas honored with 2001 John Dystel Prize.
This year's honoree is the neuropathologist Dr. John William Prineas. Educated in his native Australia, Dr. Prineas went to London in the mid-1960s for advanced medical training. He began specializing in neurology. In 1967, he came to the United States, where he was mentored by the MS clinical-care pioneer Dr. Labe Scheinberg at Albert Einstein College of Medicine. That same year, he received a postdoctoral research fellowship award from the National MS Society. "I caught the MS research bug, for life," Dr. Prineas said recently. "I find it very satisfying today to see postgraduate students being backed with fellowships as I was, and catching the same passion."
MS is a disease that takes place where the two most complicated systems in the human body interact: the central nervous system (the brain, optic nerves, and spinal cord) and the immune system. MS involves an inappropriate activation of immune-system cells, which enables them to leave the blood stream, breach a protective layer called the blood-brain barrier, enter the central nervous system, and initiate attacks on myelin, the fatty protein layer that normally protects and insulates nerve fibers, or axons. Dr. Prineas has devoted his research career to exploring what actually goes on inside MS lesions, the areas of inflammation and ultimate scarring in the central nervous system caused by this process. His research papers are now considered standard references in the MS field, characterized by outstanding scholarship and scientific rigor.
Early on, he was among the first scientists to discuss the changes in brain tissues that are now the subject of the Society's international "MS Lesion Project". Dr. Prineas is one of the senior advisors on this project.
In the late 1970s, he was the first to formally recognize that some MS lesions repair themselves. Contrary to earlier teachings, nerve fibers can and do acquire new myelin layers after an attack, a process called remyelination. He went on to demonstrate the pattern, timing, extent, and unfortunate failure of myelin replacement within MS lesions. He contributed significantly to the idea that it is myelin and not the cell that creates myelin that is attacked first--at least in the early stages of lesion development. The myelin-making cells--the oligodendrocytes--are destroyed later. At that point, new oligodendrocytes must migrate into the area for any remyelination to take place.
In a landmark study published in 1992, Dr. Prineas and his colleagues showed that new MS lesions normally remyelinate after the active inflammation and destruction stop--unless the repair process is interrupted by renewed disease activity. These insights kindle the hope that it might someday be possible to reverse MS damage.
After 25 years of research, teaching, and caring for people with MS at the VA Medical Center in East Orange, New Jersey, and the School of Medicine at University of Medicine and Dentistry New Jersey in Newark, Dr. Prineas returned to New South Wales, Australia. He is now professor of Neurology at the University of Sydney's Institute of Clinical Neurosciences.
"In the next 10 years, we will identify the MS antigen, the molecule the body is reacting against," Dr. Prineas said recently. This reaction begins when key-like structures on this molecule fit exactly into keyhole shapes on a subgroup of T-cells, white blood cells that defend the body.
"There are two different lines of investigation, both making rapid progress," he noted. "We should be able to identify the specific immunoglobulin that people with MS make (the key), and we should be able to decipher the genetics of the T-cell's receptor (which will teach us about the keyhole). Once we have that understanding, we can design treatments based on reason.
"This is an extraordinary disease and an extraordinary struggle for knowledge. Since I retired from patient care, I'm working on MS research full time."
Martha King is editor of InsideMS.
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|Date:||Jun 22, 2001|
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