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A Biomarker for Alzheimer Disease?

Arch Neurol. 2004;61:631-632.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Alzheimer disease (AD) is causally related to the buildup of -amyloid (A), a 39– to 43–amino acid protein, in the brain. Increasing evidence has implicated a biochemical association with copper in this neuropathologic condition. Copper is essential for life, mediating the activities of the respiratory chain of copper-binding proteins (cytochromes) in the mitochondria. Yet, the electron transfer chemistry of copper ion (Cu²⁺) also makes it potentially a pro-oxidant when it inappropriately reacts with oxygen (generating reactive oxygen species), proteins, or other biochemicals. For this reason, it is believed that copper ions in the cell are not in a free ionic chemical form, but rather are stringently transported and regulated by the action of several protein carriers, such as the Menkes and Wilson disease adenosine triphosphatases.

-Amyloid is a high-affinity cuproprotein, bound to copper when purified from postmortem AD-affected brain tissue.¹ The interaction of Cu²⁺ with A appears to . . . [Full Text of this Article]

Ashley I. Bush, MD, PhD
Laboratory of Oxidation Biology
Genetics and Aging Research Unit
Massachusetts General Hospital East
Bldg 114, 16th Street
Charlestown, MA 02129
(e-mail: bush@helix.mgh.harvard.edu)

Dorothea Strozyk, MD
Valhalla, NY

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