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Reduced NIH Budget Will Impact Research By Ilene Raymond Fewer federal dollars for scientific research will mean more competition for already scarce biomedical grants in fiscal year 2006. Last December, the U.S. Congress approved a modest increase in appropriations for the National Institutes of Health (NIH), the primary government agency that funds biological and medical research. But an across the board cut of one percent imposed by President Bush reduced the NIH budget to $28.6 billion. The result is that in fiscal year 2006, NIH research funds will grow by .05 percent, the smallest increase in 36 years, and .01 percent below that of 2005. When adjusted for inflation, the 2006 budget falls below that of 2003, the first time in 24 years that the NIH Research and Development portfolio drops behind inflation. "This will come as a shock to biomedical researchers, who haven't seen a declining NIH budget since 1970," says Koi Koizumi, head of research and development at the American Administration for the Advancement of Science (AAAS). "With NIH already committed to funding 2006 installments of previously awarded grants, new grants could fall dramatically." "New ideas will not be funded," says Koizumi. "Even successful researchers will find that grants are smaller and shorter." One example of this decline, cited in an AAAS report, can be seen in the National Cancer Institute, whose grant acceptance rate is expected to drop to one in 5 (19%) from a high of 33 percent in 1998. "Nationally, we are going to see a real drop in the advancement of science," says Steven Goldstein, Ph.D., professor of orthopedics and former dean of research at the University of Michigan Medical School. Goldstein expects peer review panels to lean towards more conservative projects at the cost of more risky, experimental research. Fallout may also include a drop in innovative biotechnologies that have led to profitable commercialization. "If that happens, the NIH cuts could affect not only medical progress, but the larger economy," says Goldstein. While all researchers will be pressured to produce competitive grant proposals, newly hired professors and post-docs may suffer the most from the downturn in NIH funding. Without a proven track record, young scientists may find the funding wells dry. "Fewer grants mean fewer doctors," says Ken Soprano, Vice President of Technology and Scientific Research at Temple University, who notes that as funding becomes more difficult, young people could be "driven out of research." Goldstein agrees. "When post-docs and trainees see scientists struggling with funds, they may no longer find science an attractive career." The reduced allocations will also raise tough ethical questions on which research to fund. "These are real cuts that will delay medical progress and deny hope," says David Moore, the Executive Director of the AdHoc Group for Medical Funding, a coalition who had proposed a six percent increase in the fiscal year 2006 budget and is leading a fight against future cuts. "Clearly it's a time of conflicting priorities," says Moore. "But it's not the time to begin lagging in our country's commitment to medical research, which benefits every American." For more specifics on the FY2006 NIH budget see: |
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February 2006 Issue 
Hope Against Multiple Sclerosis by Pierpaolo Basso Italian researchers report that a blockade of leptin, a hormone mainly produced by fat tissue, slows the onset and progression of experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS). In a study published in the Journal of Clinical Investigation, Giuseppe Matarese and colleagues from the Universita di Napoli "Federico II" found that leptin neutralization may prove a potential way to prevent and treat MS. MS is an autoimmune disease in which the body's T-cells attack myelin, a protective fatty substance that sheathes nerves of the central nervous system. Without this protection, signals from the brain to the body are slowed or blocked, resulting in symptoms that can affect memory, vision, and muscle coordination. Materese used two approaches: to starve mice to stave off leptin production and to neutralize leptin secretion by treating mice with anti-leptin neutralizing antibodies. In both cases EAE development was significantly inhibited by the subsequent production of anti-inflammatory cytokines, proteins which prevent and regulate organ-specific autoimmune diseases. While Materese cautions that it will that it will take three to five years to determine the effect of leptin blockage on MS, the animal results provide a path for the development and testing of new leptin-based therapies for potential treatment of MS. In recognition of his research, Materese was awarded the 2005 Rita Levi Montalcini Award, named for the Italian scientist who won the 1986 Nobel Prize. For more see: |
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