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Tau-induced memory loss in Alzheimer’s mice is reversible

Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is particularly severe. However, it app...

Unexpected new mechanism behind rheumatoid arthritis

A team of researchers at the University of Gothenburg, Sweden, has identified an enzyme that protects against inflammation and joint destruction. Made when the researchers blocked production of the enzyme GGTase-I in transgenic mice, this unexpected...

Intriguing viral link to intestinal cancer in mice

More than 50% of adults in the United States test positive for human cytomegalovirus (HCMV) infection. For most people, infection produces no symptoms and results in the virus persisting in the body for a long time. HCMV infects many cell types in t...

JCI online early table of contents: Oct. 11, 2010

EDITOR'S PICK: Intriguing viral link to intestinal cancer in mice More than 50% of adults in the United States test positive for human cytomegalovirus (HCMV) infection. For most people, infection produces no symptoms and results in the virus pers...

Scientists discover new protein that gets to the roots of obesity...

Here's good news for anyone trying to lose weight or has osteoporosis: Scientists from Maine are on the trail of a weight loss drug that may revolutionize how we treat these two conditions. In a new research report published in the September 2010 pr...

Gene therapy cuts levels of Alzheimer's protein

A molecule that naturally degrades a protein linked to Alzheimer's disease appears to reduce the levels of that protein by nearly 50 percent when delivered by gene therapy, researchers at the Salk Institute and UC San Diego have found in collaboration with researchers at the University of Kentucky. The findings appear in the March 15 issue of the Journal of Neuroscience.

Mutant protein linked to heart failure

A rare case of familial heart failure has shown that a loss of calcium regulation in heart cells may directly cause this hereditary form of the disease. The researchers who studied the case, from the Harvard Medical School lab of Christine Seidman, professor of medicine, and Jonathan Seidman, the Bugher Foundation professor of genetics, developed transgenic mice for their work that now offer a model for further investigation of heart failure and calcium signaling. The study, led by research fellow Joachim Schmitt and published in the Feb. 28 Science, suggests a specific protein target for future heart disease therapies.

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