Harvard Medical School
September 3, 2004
NEUROLOGY: Huntington's Defects Manifest Far from Damaged Brain Tissue
The ungainly movements, dementia, and mood swings that characterize Huntington's disease are the result of a single mutation--one that kills neurons in a specific brain structure, the striatum. It now appears that this mutation triggers defects in other areas of the brain, and even in other parts of the body, yet these other cells find a way to cope. The discovery, described by (left to right) Ole Isacson, Hyemyung Seo, and Kai-Christian Sonntag in the September Annals of Neurology, could provide clues to treating this incurable disease by protecting striatal neurons in Huntington's patients.
PUBLIC HEALTH: Sugary Drinks Raise Risk of Obesity, Type 2 Diabetes
Sugar-sweetened sodas and faux fruit drinks increased the risk of type 2 diabetes in adults, according to a study in the Aug. 25 Journal of the American Medical Association by HSPH researchers Matthias Schulze, Frank Hu (at right), and their colleagues. Weight gain accounted for only half the additional risk. "If people just cut their soft drink consumption, society can go a long way toward reducing the rates of obesity and diabetes," Hu said.
NEUROMUSCULAR RESEARCH: Action Uncovered in Mutant Protein's Link to Nerve Cell Death in ALS
Mutant forms of the common protein SOD1 have been tied to a subset of cases of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. But how the protein contributes to the disorder's lethal progress has remained unclear. Robert Brown, Piera Pasinelli, and colleagues report in the July 8 Neuron that mutant SOD1 appears to enlist another protein in doing its damage. The pair targets motor neurons, forming clumps around the cells' mitochondria and breaking down the organelle membranes, resulting in cell death. Why the killer clumps form only in motor neurons is still unknown.
How Does Insurance Affect the Risk of Premature Death Among the Near-elderly?
A Lot for Whites, a Little for Blacks