Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse

Dale Schenk (), Robin Barbour, Whitney Dunn, Grace Gordon, Henry Grajeda, Teresa Guido, Kang Hu, Jiping Huang, Kelly Johnson-Wood, Karen Khan, Dora Kholodenko, Mike Lee, Zhenmei Liao, Ivan Lieberburg, Ruth Motter, Linda Mutter, Ferdie Soriano, George Shopp, Nicki Vasquez, Christopher Vandevert, Shannan Walker, Mark Wogulis, Ted Yednock, Dora Games and Peter Seubert
Additional contact information
Dale Schenk: Elan Pharmaceuticals
Robin Barbour: Elan Pharmaceuticals
Whitney Dunn: Elan Pharmaceuticals
Grace Gordon: Elan Pharmaceuticals
Henry Grajeda: Elan Pharmaceuticals
Teresa Guido: Elan Pharmaceuticals
Kang Hu: Elan Pharmaceuticals
Jiping Huang: Elan Pharmaceuticals
Kelly Johnson-Wood: Elan Pharmaceuticals
Karen Khan: Elan Pharmaceuticals
Dora Kholodenko: Elan Pharmaceuticals
Mike Lee: Elan Pharmaceuticals
Zhenmei Liao: Elan Pharmaceuticals
Ivan Lieberburg: Elan Pharmaceuticals
Ruth Motter: Elan Pharmaceuticals
Linda Mutter: Elan Pharmaceuticals
Ferdie Soriano: Elan Pharmaceuticals
George Shopp: Elan Pharmaceuticals
Nicki Vasquez: Elan Pharmaceuticals
Christopher Vandevert: Elan Pharmaceuticals
Shannan Walker: Elan Pharmaceuticals
Mark Wogulis: Elan Pharmaceuticals
Ted Yednock: Elan Pharmaceuticals
Dora Games: Elan Pharmaceuticals
Peter Seubert: Elan Pharmaceuticals

Nature, 1999, vol. 400, issue 6740, 173-177

Abstract: Abstract Amyloid-β peptide (Aβ) seems to have a central role in the neuropathology of Alzheimer's disease (AD)1. Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes2,3. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Aβ42)4,5,6,7,8, which is the predominant form found in the amyloid plaques of Alzheimer's disease9,10. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner11,12. In the present study, transgenic animals were immunized with Aβ42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-β deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of β-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-β may be effective in preventing and treating Alzheimer's disease.

Date: 1999
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DOI: 10.1038/22124

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