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NEUROLOGY: Alzheimer's Plaques Reversed in Mice by Blocking Cholesterol Pathway
It has been almost 100 years since Alois Alzheimer described the senile plaques characterizing the disease that now bears his name. Since then, researchers have been trying to figure out how to prevent the build-up of those plaques and the associated neurodegeneration. In the Oct. 14 Neuron, Dora Kovacs (at right), Henri Huttunen, and colleagues describe a novel approach that works remarkably well in young mice with Alzheimer's-like pathology. By inhibiting an enzyme that redistributes cholesterol in the cell, the scientists have reduced the plaque burden by up to 99 percent and improved spatial learning and memory in the most afflicted animals. The findings could lead toward similar treatments in humans.

METABOLISM: Cellular Stress Appears to Link Obesity, Diabetes
Inside fat and liver cells of overweight mice, HSPH researchers may have found a pivotal mechanism that turns extra pounds into insulin resistance and type 2 diabetes. Gökhan Hotamisligil and colleagues report in the Oct. 15 Science that the cells appear to react to extra fat with a stress response, unleashing insulin saboteurs. It all begins in the endoplasmic reticulum, a membranous network enclosing the nucleus and known as the cellular protein-finishing factory.

PATHOLOGY: Blood Flow Mechanics Affect Genetics in Vascular Cells
The constant forces of rushing blood can influence the way that endothelial cells lining blood vessels function. In a study published in the Oct. 12 Proceedings of the National Academy of Sciences, a team led by Michael Gimbrone (at right) and Guillermo García-Cardeña shows how different patterns of shear stress change gene expression in these cells. The findings may help explain why atherosclerotic plaques tend to form in the branches of arteries, not on the straightaways.

STRUCTURAL BIOLOGY: Interdisciplinary Team Yields High-res Clathrin Model
The transport protein clathrin continuously assembles and disassembles large, cagelike structures that capture, carry, and release nutrients and other cargo inside cells. Three HMS investigators in the Center for Molecular and Cellular Dynamics pooled their expertise in biochemistry, physics, and computing to produce the most detailed structure to date of a complete clathrin lattice. The model, put together in the labs of Stephen Harrison (at right), Thomas Walz, and Tomas Kirchhausen and published online in the journal Nature, reveals for the first time the precise molecular contacts that drive self-assembly and disintegration of the transport vesicle.