Researchers Map Physical Basis of Dyslexia
A Yale research team funded by the National Institute of Child Health and Human Development has used sophisticated brain imaging technology to show that there is decreased functioning while performing reading tasks in certain brain regions of individuals with the most common form of dyslexia. The study appeared in the Mar. 3 issue of the Proceedings of the National Academy of Sciences.
In their study, the researchers used a technology known as functional magnetic resonance imaging (fMRI), which produces computer-generated images of the brain while it is performing intellectual tasks. With fMRI, the team produced images of an impairment in the brains of dyslexic readers that became apparent when they tried to perform tasks that would require a firm command of the ability to decipher words phonetically.
"If you have a broken arm, we can see that on an X-ray," said the study's first author, Dr. Sally E. Shaywitz of Yale University School of Medicine. "These brain activation patterns now provide us with hard evidence of a disruption in the brain regions responsible for reading -- evidence for what has previously been a hidden disability."
Shaywitz explained that the words we speak are made up of individual sounds called phonemes. In spoken language, the brain automatically combines these sounds to form words. To make normal conversation possible, such sound pieces are strung together rapidly -- about 8 to 10 per second -- and blended so thoroughly that it's often impossible to separate them.
For people with dyslexia, the problem arises in converting this natural process to print. Written English is a kind of code: The 26 letters of the alphabet, either singly or in combination with other letters, stand for the 44 letter phonemes in spoken English. Dyslexic readers have extreme difficulty with phonological awareness (breaking spoken words into their component sounds) and with phonetics (the ability to match these letter sounds to the letters that represent them).
Dyslexic readers showed reduced activity in a large brain region that links the visual cortex and visual association areas (angular gyrus) to the language regions in the superior temporal gyrus (Wernike's area).
New Drug Treatment for Iron Overload?
Researchers may have found a better drug treatment to remove iron from patients who have too much. Too much iron damages vital organs, especially the liver, heart, and pancreas. That's a problem for as many as 50,000 people in the United States who need regular blood transfusions for anemias such as Cooley's anemia and some patients with sickle cell disease.
The small intestine usually regulates how much iron is absorbed into the blood, but transfusions bypass this safety mechanism, sending iron-rich blood straight to the bloodstream. To rid the body of extra iron, patients use a chelator, a drug that attaches to iron so it can escape body cells and be excreted in stool and urine. Unfortunately, the standard chelator, deferoxamine (DFO), is expensive and has effects patients don't like.
The drug HBED, or hydroxybenzylethylenediamine diacetic acid, removed up to 3 times more iron than DFO when tested in normal rats and in primates overloaded with iron. The study appeared in the Feb. 15 issue of Blood and was funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases.
"We've been desperate to offer something better to patients," said Dr. Raymond J. Bergeron, lead author of the study and a medicinal chemist at the University of Florida College of Pharmacy in Gainesville. "We don't want to raise false hopes before we've done more studies, but primates are a magnificent predictor of what will happen in people, and this looks great in the primate. It's hard not to get excited."
Strategy for Preventing Periodontal Disease
Preventing two key cytokines from attaching to their natural receptors on cells may stop the progression of periodontal disease, say scientists supported by the National Institute of Dental Research. The findings confirm that IL-1 and TNF -- two proteins made by immune cells -- are major players in periodontal destruction. Blocking their activity may inhibit periodontal bone loss by as much as 60 percent.
Working in a primate model, the researchers were able to prevent IL-1 and TNF from attaching to cell receptors by injecting soluble receptors to the proteins into the gum area. Instead of locking onto their natural receptors on cells, IL-1 and TNF clung to the soluble receptors, which prevented them from making contact with cells and signaling the start of the destructive inflammatory process. The scientists note that 6 weeks after the injections there was a drastic decrease in the number of inflammatory cells in the gum and alveolar bone area, demonstrating that the soluble receptors effectively interfered with the disease process.
The study appeared in the January 1998 issue of the Journal of Immunology.
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