Scientists who study Alzheimer disease have long debated whether the
cascade of pathological events that leads to neurodegeneration is triggered
by the amyloid-β (Aβ) peptide when it is first produced in diseased
neurons or by the accumulation of amyloid plaques outside the cells. A study
by an international team of researchers from Switzerland, Belgium, and the
United States now gives support to those who favor amyloid deposits as a key
factor in disease progression.
In the study, the researchers used transgenic mice that express a mutated
version amyloid precursor protein (the forerunner to Aβ) to study the
formation of plaques. They found that plaques formed within normal murine
brain tissue grafted into the brains of the mutant mice, and that the grafted
tissue also displayed other signs of amyloid pathology and neurodegeneration.
Stephenson J. Mosquitoes and Malaria. JAMA. 2003;289(10):1234. doi:10.1001/jama.289.10.1234-a