We studied the presence of β-amyloid (βA) cortical deposits in a group of young (n = 7), aged no-cognitively-impaired (NCI, n = 14), and aged cognitively-impaired (CI, n = 5) dogs. βA was visualized by immunohistochemistry. The extension of the deposits was estimated by area fraction fractionator in one frontal lobe section per dog.
No βA labeling could be detected in the brain of young dogs. Extensive βA deposits were found in all the aged-CI dogs. Additionally, seven aged-NCI dogs presented moderate to high βA deposits in spite of no apparent cognitive symptoms. The βA deposits appeared as diffuse plaques that spread across the deep cortical layers from the limit with the subjacent white matter. In the 5 aged-CI dogs these plaques were also seen in more superficial cortical layers where they tended to acquire a denser and better delimited appearance. Many small-diameter cortical blood vessels were intensely stained in 8 of the 12 dogs with βA deposits, including 4 without cognitive impairment. In contrast, seven aged dogs were free of cortical βA deposits. These results suggest that βA deposits is not a mere consequence of normal aging but exogenous and/or genetic factors could determine the susceptibility of the individuals to develop amyloid pathology at a given age. The finding of βA angiopathy and a moderate to heavy βA burden in some aged animals lacking a positive diagnostic of cognitive impairment reminds similar reports on the presence of extensive βA deposits in non demented human brains. It is possible that early symptoms of the canine counterpart of AD could pass unnoticed to the owners and underline the importance to found reliable biomarkers for the disease.