β-amyloid(Aβ) is a predominant component of senile plaques, one central pathological hallmark of Alzheimer's disease. Immunization with Aβ causes a marked reduction of Aβ burden and its associated pathologies in brain. A clearance of the preexisting plaques has been observed in transgenic mice, with an inhibition of lesion of cognitive functions. No signs of an immune-mediated response could be detected to endogenous Aβ peptide of mice. The chronic inflammatory response resulted from the immunization itself has not obviously impaired functions of central nerve system.