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Vol. LXI, No. 13
June 26, 2009
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Digest

  NIH scientists have gained a major insight into how the rogue protein responsible for mad cow disease and related neurological illnesses destroys healthy brain tissue.  
  NIH scientists have gained a major insight into how the rogue protein responsible for mad cow disease and related neurological illnesses destroys healthy brain tissue.  

NIH Researchers Discover How Prion Protein Damages Brain Cells

Scientists at NIH have gained a major insight into how the rogue protein responsible for mad cow disease and related neurological illnesses destroys healthy brain tissue.

“This advance sets the stage for future efforts to develop potential treatments for prion diseases or perhaps to prevent them from occurring,” said Dr. Duane Alexander, director of the National Institute of Child Health and Human Development, where the study was conducted.

The researchers discovered that the protein responsible for these disorders, known as prion protein (PrP), can sometimes wind up in the wrong part of a cell. When this happens, PrP binds to mahogunin, a protein believed to be essential to the survival of some brain cells. This binding deprives cells in parts of the brain of functional mahogunin, causing them to die eventually. The scientists believe this sequence of events is an important contributor to the characteristic neurodegeneration of these diseases.

The findings were published in the June 12 issue of the journal Cell. The study was conducted by Drs. Oishee Chakrabarti and Ramanujan S. Hegde of the Cell Biology and Metabolism Program.

NIAID Outlines Research Agenda for Universal, Voluntary HIV Testing, Treatment

Could a global program of universal, voluntary, annual HIV testing and immediate treatment for those who test positive effectively extinguish the HIV pandemic? Is such a program feasible? In the June 10 issue of the Journal of the American Medical Association, HIV/AIDS research leaders at the National Institute of Allergy and Infectious Diseases set forth a research agenda to answer these and other questions that may help shape the future of HIV prevention.

The inspiration for the research agenda is a mathematical modeling study published by scientists from the World Health Organization in The Lancet in January 2009. The model by Granich et al. predicts that within 10 years of implementation, a program of universal, voluntary, annual HIV testing and immediate treatment for those who test positive could reduce HIV incidence from 20 new cases per 1,000 people per year—the current rate in places like South Africa—to less than 1 case per 1,000 per year. Further, the model predicts that this strategy, colloquially called “test and treat,” could end the pandemic within 50 years. Some 33 million people globally are infected with HIV today.

“Given these conclusions, test and treat potentially could represent an important public health strategy for fighting HIV/AIDS,” said NIAID director Dr. Anthony Fauci. “However, the WHO model is based on numerous assumptions that need to be tested and also raises concerns about individual rights, cost effectiveness and other critical issues that require broad public debate.”

Test and treat is one component of a three-part strategy that NIAID is examining to control the HIV/AIDS pandemic. The other parts are pre-exposure prophylaxis and developing ways to control and eliminate the cells carrying latent virus, potentially curing people of HIV.

Genetic Variant Associated with Resistance to Chemo Drug in Women with Breast Cancer

Researchers have found links between individuals’ genetics and their response to treatment with chemotherapy. The findings, by researchers at the National Cancer Institute and colleagues, show how a genetic variant, located in the SOD2 gene, may affect how a person responds to the chemotherapy drug cyclophosphamide. Cyclophosphamide is used in the treatment of breast and other cancers.

The SOD2 gene produces a key protein that protects cells from damage by molecules known as reactive oxygen species, or free radicals. Reactive oxygen species are produced by normal cellular processes and the action of some chemotherapy drugs. The findings represent the first preliminary evidence pointing toward a mechanism and a potential biomarker for cyclophosphamide resistance in breast cancer patients. The study appeared online June 9 in Clinical Cancer Research.

“This study shows how, with the progress of individualized medicine, a diagnostic test may be developed that determines whether a patient has certain genetic variations that may modify the effect of certain chemotherapies,” said study author Dr. Sharon Glynn of NCI’s Center for Cancer Research

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