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William R. Markesbery, MD; Mark A. Lovell, PhD

Arch Neurol. 2007;64(7):954-956.

Free radical–mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. Previous studies have shown oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage Alzheimer disease. Recent studies on patients with amnestic mild cognitive impairment who have undergone autopsy have shown increased lipid peroxidation as well as protein, DNA, and RNA oxidation in multiple brain regions. These studies establish oxidative damage as an early event in the pathogenesis of Alzheimer disease that can serve as a therapeutic target to slow the progression or perhaps the onset of the disease.

Author Affiliations: Departments of Neurology (Dr Markesbery), Pathology and Laboratory Medicine (Dr Markesbery), and Chemistry (Dr Lovell), Alzheimer's Disease Center (Drs Markesbery and Lovell), and Sanders-Brown Center on Aging (Drs Markesbery and Lovell), University of Kentucky, Lexington.

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