|
||
 |
||
New Administrative Leader Takes Reins at CUMC
research briefs
| Possible Link Between Stroke and Alzheimer’s Found A newly discovered pathway in the brain may help explain why stroke nearly doubles the risk of developing Alzheimer’s disease. Alzheimer’s is believed to be caused by toxic amyloid beta (Aß) peptides that accumulate in the brain. Aß levels are known to increase after a stroke, but it is not known why, says Karen Duff, PhD, professor of pathology in psychiatry and the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain. Dr. Duff’s new study found that in cells and transgenic mice, Aß levels rise when there is an increase in another protein, p25, which also has been previously linked to stroke. One component of the pathway that connects p25 and Aß may be a good target for treatments aimed at preventing post-stroke Alzheimer’s, the researchers also discovered. When the activity of this component (called cdk5) was restrained, toxic Aß levels dropped. Dr. Duff cautions, however, that it is still unclear if stroke actually triggers the p25/cdk5 pathway. Her lab is currently looking for signs of activation in stroke patients. The work was supported by the NIH and the Alzheimer’s Association. Neuron 57(5): 680-690 “Speed” May Nurture AIDS-related Infections Methamphetamine – colloquially known as “crystal,” “tina,” “meth,” or “speed” – may hasten the development of AIDS in HIV-infected individuals by weakening the immune system, according to a new study by Zsolt Talloczy, PhD, associate research scientist, and David Sulzer, PhD, associate professor, in the Department of Neurology, and their colleagues. Use of methamphetamine has reached epidemic proportions in the past decade. About 5 percent of the U.S. population has used the drug at least once, and there are an estimated 35 million users around the world. Methamphetamine users are twice as likely to be infected with HIV as non-users. The new study found that methamphetamine impairs the ability of immune cells to defend against AIDS-related pathogens by increasing pH inside the cells. The change in pH prevents the cells from engulfing and destroying bacteria and fungi and from activating other parts of the immune response. PLoS Pathogens 4(2): e28 This work was supported by the NIH, the Parkinson’s Disease Foundation, and the Einstein/Montefiore Medical Center for AIDS Research. Study Faults Immune System in Lung Disease An aberrant immune response triggers the development of one of the first events in pulmonary arterial hypertension (PAH), according to a team led by Gabriele Grunig, DVM, assistant professor of microbiology. PAH is a rare but deadly disease of unknown origin that has no cure. PAH occurs when small pulmonary arteries become constricted, forcing the heart to work harder to pump blood through the lungs. Most patients die from heart failure within three years of diagnosis. Though the immune system has been a suspect in PAH for more than four decades – because many cases of PAH occur in people with other immune conditions such as lupus, rheumatoid arthritis, and HIV infection – no direct experimental proof has linked the two until now. Dr. Grunig and her colleagues found that mice exposed intermittently to various inhaled antigens generate a T cell response that leads to severe thickening of pulmonary arteries, one of the first events in the development of PAH. Mice with arteries surrounded by thick layers of smooth muscle cells, however, did not have hypertension. Dr. Grunig says that more work is needed to determine how thickened arteries lead to PAH. Journal of Experimental Medicine 205(2): 361. The work was funded by the Flight Attendant Medical Research Institute, the American Heart Association, the American Lung Association, Schering-Plough Biopharma, and the Stony Wold-Herbert Fund. |
