Prevention and Reduction of AD‐type Pathology in PDAPP Mice Immunized with Aβ1–42

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 Aβ_1–42, which essentially prevented amyloid deposition; astrocytosis was dramatically reduced and there was reduction in Aβ‐induced inflammatory response as well. Aβ_1–42 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.