Vaccinations with amyloid-beta peptide (AB) can dramatically reduce amyloid
deposition in a transgenic mouse model of Alzheimer's disease(1). To deter
mine if the vaccinations had deleterious or beneficial functional consequen
ces, we tested eight months of A beta vaccination in a different transgenic
model for Alzheimer's disease in which mice develop learning deficits as a
myloid accumulates(2,3). Here we show that vaccination with A beta protects
transgenic mice from the learning and age-related memory deficits that nor
mally occur in this mouse model for Alzheimer's disease. During testing for
potential deleterious effects of the vaccine, all mice performed superbly
on the radial-arm water-maze test of working memory. Later, at an age when
untreated transgenic mice show memory deficits, the A beta -vaccinated tran
sgenic mice showed cognitive performance superior to that of the control tr
ansgenic mice and, ultimately, performed as well as nontransgenic mice. The
A beta -vaccinated mice also had a partial reduction in amyloid burden at
the end of the study. This therapeutic approach may thus prevent and, possi
bly, treat Alzheimer's dementia.