Bj. Cummings et al., BETA-AMYLOID ACCUMULATION IN AGED CANINE BRAIN - A MODEL OF EARLY PLAQUE-FORMATION IN ALZHEIMERS-DISEASE, Neurobiology of aging, 14(6), 1993, pp. 547-560
We characterized eight aged beagles (maintained from birth in a labora
tory colony) and one black Labrador using Bielschowsky's, thioflavine
S, and Congo red staining, and antibodies to the beta-amyloid peptide,
dystrophic neurites, and other plaque components. All plaques within
these canine brains were of the diffuse subtype and were neither thiof
lavine S- nor Congo red-positive. The majority of plaques in the entor
hinal cortex contained numerous neurons within them while plaques in t
he dentate gyrus did not. beta-Amyloid immunoreactivity was also prese
nt within select neurons and neuronal processes and was detected as a
diffuse linear zone corresponding to the terminal fields of the perfor
ant path. There was no significant correlation between extent of beta-
amyloid accumulation and neuron number in entorhinal cortex. Neither t
au-1, PHF-1, nor SMI-31-immunostaining revealed dystrophic fibers, con
firming the classification of these plaques as diffuse. Canine plaques
did not appear to contain bFGF- or HS-positive immunostaining. This m
ay explain why neuritic involvement was not detected within these cani
ne plaques. It is possible that the beta-amyloid within the canine bra
in has a unique primary structure or may not be in an assembly state t
hat adversely affects neurons.