Abstract: In AD certain brain structures contain a pathological density of Aβ protein deposited into plaques. The effect of genetic mutations found in early onset AD patients was an overproduction of Aβ42, strongly suggesting that overproduction of Aβ42 is associated with AD. We hypothesized that an immunological response to Aβ42 might alter its turnover and metabolism. Young PDAPP transgenic mice were immunized with Aβ1–42, which essentially prevented amyloid deposition; astrocytosis was dramatically reduced and there was reduction in Aβ-induced inflammatory response as well. Aβ1–42 immunization also appeared to arrest the progression of amyloidosis in older PDAPP mice. Aβ immunization appears to increase clearance of amyloid plaques, and may therefore be a novel and effective approach for the treatment of AD.