Reducing Amyloid Beta Levels in a Mouse Model of Alzheimer's

This is one of a number of approaches in recent years that has significantly reduced the levels of amyloid beta in the brain in the mouse version of Alzheimer's disease used for research. As for the others, it remains to be seen whether it is a suitable basis for a human therapy. Even if so, like much of the approach of modern medicine for age-related conditions, it isn't addressing causes, only trying to patch over consequences:

One of the main characteristics of Alzheimer's disease is the production in the brain of a toxic molecule known as amyloid beta. Microglial cells, the nervous system's defenders, are unable to eliminate this substance, which forms deposits called senile plaques.

[Researchers] identified a molecule that stimulates the activity of the brain's immune cells. The molecule, known as MPL (monophosphoryl lipid A), has been used extensively as a vaccine adjuvant [for] many years, and its safety is well established.

In mice with Alzheimer's symptoms, weekly injections of MPL over a twelve-week period eliminated up to 80% of senile plaques. In addition, tests measuring the mice's ability to learn new tasks showed significant improvement in cognitive function over the same period.

The researchers see two potential uses for MPL. It could be administered by intramuscular injection to people with Alzheimer's disease to slow the progression of the illness. It could also be incorporated into a vaccine designed to stimulate the production of antibodies against amyloid beta. "The vaccine could be given to people who already have the disease to stimulate their natural immunity. It could also be administered as a preventive measure to people with risk factors for Alzheimer's disease."



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