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Prevention and Reduction of AD‐type Pathology in PDAPP Mice Immunized with Aβ 1–42
Author(s) -
GAMES DORA,
BARD FREDERIQUE,
GRAJEDA HENRY,
GUIDO TERRY,
KHAN KAREN,
SORIANO FERDIE,
VASQUEZ NICKI,
WEHNER NANCY,
JOHNSONWOOD KELLY,
YEDNOCK TED,
SEUBERT PETER,
SCHENK DALE
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06936.x
Subject(s) - astrocytosis , beta (programming language) , genetically modified mouse , amyloidosis , immunology , amyloid (mycology) , immunization , pathological , transgene , medicine , biology , pathology , antigen , genetics , immunohistochemistry , computer science , gene , programming language
A bstract : 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 Aβ 42 , strongly suggesting that overproduction of Aβ 42 is associated with AD. We hypothesized that an immunological response to Aβ 42 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.