Amyloid β 1-42 deposits do not lead to Alzheimer's neuritic plaques in aged dogs

Author:

WISNIEWSKI Thomas1,LALOWSKI Maciej2,BOBIK Marketta3,RUSSELL Michael3,STROSZNAJDER Joanna4,FRANGIONE Blas2

Affiliation:

1. Department of Neurology, New York University Medical Center, 550 First Avenue TH 427, New York, NY 10016, U.S.A.

2. Department of Pathology, New York University Medical Center, 550 First Avenue TH 427, New York, NY 10016, U.S.A.

3. Department of Anesthesiology and Otolaryngology, University of California at Davis, Davis, CA, U.S.A.

4. Polish Academy of Science, Laboratory of Cellular Signalling, Medical Research Center, Warsaw, Poland

Abstract

In Alzheimer's disease, amyloid β (Aβ) is deposited in senile plaques and amyloid angiopathy. Longer Aβ peptides, which extend to residue 42 (Aβ42), have been suggested to be critical for the seeding of amyloid. Aged dogs develop cerebral vessel amyloid and parenchymal preamyloid lesions. Preamyloid in humans is related to senile plaques, whereas in dogs such progression is rare. We evaluated the composition of aged canine vessel amyloid and preamyloid both biochemically and immunohistochemically. The vessel amyloid extended mainly to residue 40 (Aβ40), while preamyloid contained a mixture of Aβ17-42 and Aβ42, with minimal Aβ40. Our results suggest other factors besides Aβ42 are important for neuritic plaque formation.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

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