Tag Archives: amyloid-β
Researchers have identified within neurons a series of molecular interactions — known as a pathway — that can dampen the production of the Alzheimer’s protein amyloid-β. These results suggest a new route in the search for therapies for this degenerative disease. More »
Researchers identify a molecular bridge between amyloid-β and chronic inflammation, two hallmarks of Alzheimer’s. That bridge, a molecular cascade known as the contact system, suggests the possibility of a simple blood test that could diagnose the disease early and non-invasively.
The brains of Alzheimer’s mice treated with the compound RU-505 showed less inflammation and better blood flow than those of untreated mice. The treated mice also performed better on memory tests. More »
A molecule that activates the cell’s natural recycling program may flush away the protein fragments that accumulate and form senile plaques in Alzheimer’s disease. New research suggests that stimulating this activity, either through drugs or natural processes, may improve the quality of life for people with diseases caused by built-up proteins in the brain. More »
Alzheimer’s disease isn’t just about twisted brain cells, but also the blood vessels that feed those neurons. Previous research at Rockefeller University showed that the most common element of telltale plaque deposits in Alzheimer’s brains leads to the formation of tougher blood clots, which could choke off oxygen flow to neurons. The new research shows how these clots are formed, suggesting a target for a drug that might prevent them. More »
Rockefeller researchers report that the cancer drug Gleevec reduces Alzheimer’s plaques in a mouse model of the disease by binding to a molecule called gamma-secretase activating protein, or GSAP. By knocking out the gene that produces GSAP, the researchers reduced the primary component of senile plaques. They say that the development of compounds that work like Gleevec and target GSAP could revolutionize the treatment of this disease. More »
Alzheimer’s disease isn’t just about twisted brain cells. It’s also about the blood vessels that feed those neurons. New research at Rockefeller University has shown how the most common element of the plaque deposits found outside the brain cells of Alzheimer’s patients interacts with a blood clotting agent and causes clots to form faster and become harder to break down. The scientists suggest new drugs that would target this association could potentially treat what is increasingly recognized as a crucial element of the disease, the vascular component. More »