Much of Alzheimer’s research has focused on the role of a protein, amyloid-beta, found at high levels in the brains of Alzheimer’s patients and which coagulates into plaques. Researcher Ashley Bush, a Harvard Medical School associate professor of psychiatry at Massachusetts General Hospital, believes that something else causes Alzheimer’s dementia: oxidation of trace metals in the brain. According to Bush’s model, oxidative damage results from an improper interaction of amyloid-beta with copper and zinc, which exist naturally in the neocortex of the brain and have been found at elevated levels in Alzheimer’s plaques. Though it has been difficult for Bush and his colleagues to gain acceptance for the ideas they have been developing for years, a new study in mice offers evidence to support Bush’s model. Mice with an overabundance of amyloid-beta were treated with clioquinol, a retired antibiotic; the drug worked to reduce deposits of amyloid-beta and had the effect of improving the general health of the mice. Bush credits the effects to reduced oxidation.