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Office of Neuroscience Research > WUSTL Neuroscience News > Alzheimer’s damage in mice reduced with compound that targets APOE gene

Alzheimer’s damage in mice reduced with compound that targets APOE gene



From the WashU Newsroom...

People who carry the APOE4 genetic variant face a substantial risk for developing Alzheimer’s disease.

Now, researchers at Washington University School of Medicine in St. Louis have identified a compound that targets the APOE protein in the brains of mice and protects against damage induced by the Alzheimer’s protein amyloid beta.

“Scientists have been interested in APOE for years but there are only a few examples where researchers have targeted it with a compound in living animals,” said senior author David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. “Our findings indicate that APOE is not just involved in Alzheimer’s risk and disease progression, but it could potentially be a real target for treatment or prevention.”

The study is published Dec. 6 in the journal Neuron.

Alzheimer’s, which affects one in 10 people over age 65, is marked by brain plaques made of a sticky protein known as amyloid beta. The plaques start forming in the brains of Alzheimer’s patients years before the characteristic symptoms of memory loss and confusion appear. APOE4 raises the risk of Alzheimer’s partly by encouraging amyloid beta to collect into damaging plaques.

Holtzman, first author and MD/PhD student Tien-Phat Huynh, and colleagues studied mice genetically prone to develop amyloid plaques and that carry the human APOE4 genetic variant. People with APOE4 face up to 12 times the risk of developing Alzheimer’s than the general population.

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