Faculty Collaboration Database

The progression of beta-amyloid deposition in the frontal cortex of the aged canine. Brain Res 1997 Nov 07;774(1-2):35-43

Date

02/06/1998

Pubmed ID

9452189

DOI

10.1016/s0006-8993(97)81684-8

Scopus ID

2-s2.0-0031558637 (requires institutional sign-in at Scopus site)   80 Citations

Abstract

Brains from 41 aged canines (> or = 10 years of age) were examined immunohistochemically to characterize the laminar distribution and age-related progression of beta-amyloid (A beta) in frontal cortex. We classified the A beta patterns into four distinct types. Type I was characterized by small, faint deposits of A beta in deep cortical layers. Type II consisted of diffuse deposits of A beta mainly in layers V and VI. Type III had both dense plaques in superficial layers, and diffuse deposits in deep layers. Finally, Type IV had solely dense plaques throughout all layers of cortex. We compared the A beta distribution pattern between the Old canines (10-15 years, n = 22) and the Very Old canines (> 15 years, n = 19). The Old group primarily had negative staining, or Type I and Type II patterns of amyloid deposition (73%). Conversely, the Very Old group had predominantly Types II, III and IV deposits (89.5%), a difference that was significant (P < 0.05). We suggest that A beta deposition in canine frontal cortex is a progressive age-related process beginning with diffuse deposits in the deep cortical layers followed by the development of deposits in outer layers. In support of this hypothesis, the deeper layer diffuse plaques in the Very Old group of dogs also contain the largest proportion of beta-amyloid with an isomerized aspartic acid residue at position 7, indicating that these deposits had been present for some time. We also observed fiber-like A beta immunoreactivity within regions of diffuse A beta deposits. These fibers appeared to be degenerating neurites, which were negative for hyperphosphorylated tau. Therefore, these fibers may represent a very early form of neuritic change that precede tau hyperphosphorylation or develop by an alternative pathway.

Author List

Satou T, Cummings BJ, Head E, Nielson KA, Hahn FF, Milgram NW, Velazquez P, Cribbs DH, Tenner AJ, Cotman CW

Author

Kristy Nielson PhD Professor in the Psychology department at Marquette University

MESH terms used to index this publication - Major topics in bold

Aging
Alzheimer Disease
Amyloid beta-Peptides
Animals
Disease Models, Animal
Disease Progression
Dogs
Female
Frontal Lobe
Immunohistochemistry
Male
Nerve Degeneration
Tissue Distribution