This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Brian Vastag

JAMA. 2001;285:874.

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

For several years, researchers have puzzled over the role of brain plaques in Alzheimer disease. Are they cause or effect? By detailing a mechanism of memory disruption, new research from the National Institute of Environmental Health Sciences supports the hypothesis that plaques cause the disease.

Jerrel Yakel, PhD, and colleagues report that the major component of the plaques, called -amyloid peptide, binds to a key memory signaling receptor, the nicotinic acetylcholine receptor, in the hippocampus of rats. The hippocampus is the seat of memory and emotion in the brain. By blocking the receptors, the researchers say that the peptides inhibit the cascade of signals thought to be important in learning and memory formation.

The researchers are hopeful that their finding will lead to drugs that stem the peptide's affinity for the receptors. "Knowing how the disease process works makes it more likely that medical science will find ways . . . [Full Text of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?