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 β-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.