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Archive - Aug 2014

Scientists Discover Biochemical Mechanisms Contributing to Fibromuscular Dysplasia

An important step has been made to help better identify and treat those with fibromuscular dysplasia (FMD). FMD causes both an abnormal narrowing and enlarging of medium-sized arteries in the body, which can restrict blood flow to the kidneys and other organs causing damage. In a new report appearing in the August 2014 issue of The FASEB Journal, scientists provide evidence that that FMD may not be limited to the arteries as currently believed. In addition, the scientists show a connection to abnormalities of bones and joints, as well as evidence that inflammation may be driving the vascular disease in FMD patients. "Having medical treatment options for FMD, or for people who may be susceptible to FMD, will improve their quality of life by preventing vascular complications," said Nazli B. McDonnell, M.D., Ph.D., a researcher involved in the work from the National Institute on Aging at the National Institutes of Health in Baltimore, Maryland. "Recognizing the additional features of FMD, namely those involving the joints and bones, may help us to design better treatments for these ancillary symptoms that were previously thought to be independent of FMD." To make this discovery, Dr. Nazli and colleagues recruited patients with FMD and performed physical exams. Vascular imaging and bone density studies were also conducted. Researchers measured specific proteins in the blood that indicated inflammation activation of the transforming growth factor-beta (or TGF-beta) pathway. Patient skin biopsies also were collected to grow dermal fibroblast cell lines, which were studied for TGF-beta pathway and inflammatory biomarkers and were compared to age-, sex-, and BMI-matched controls that did not have FMD. "FMD is a serious blood vessel disease for which we know little," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal.

Potential Basis for the Treatment and Prevention of Parkinson’s Disease

Parkinson’s disease affects neurons in the substantia nigra brain region – their mitochondrial activity ceases and the cells die. In an open-access article published online on August 1, 2014 in The Company of Biologists/Biology Open, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, show that supplying D-lactate or glycolate, two products of the gene DJ-1, can stop and even counteract this process: Adding the substances to cultured HeLa cells and to cells of the nematode C. elegans restored the activity of mitochondria and prevented the degeneration of neurons. Thee team also showed that the two substances rescued the toxic effects of the weed killer Paraquat. Cells that had been treated with this herbicide, which is known to cause a Parkinson's-like harm of mitochondria, recovered after the addition of the two substances. Both glycolic and D-lactic acids occur naturally in unripe fruits and certain kinds of yoghurt. Drs. Teymuras Kurzchalia and Tony Hyman both have labs at the Max Planck Institute of Molecular Cell Biology and Genetics with rather different research programs – but both happened to stumble upon the gene DJ-1 and joined forces. This gene, originally thought of as an oncogene, has been linked to Parkinson’s disease since 2003. Recent studies showed that DJ-1 belongs to a novel glyxolase family. The major function of these genes is assumed to be the detoxification of aggressive aldehyde by-products from mitochondrial metabolism. The Dresden research team has now shown that the products of DJ-1, D-lactate and glycolate, are actually required to maintain the high mitochondrial potential and thus can prevent the degeneration of neurons implicated in Parkinson’s disease.