|The process of neurodegeneration displays some common morphological characteristics, most of which are jointly observed in the brains of most mammalian species.
In the canine brain, neurodegeneration is frequently typified by an extensive beta-amyloid (A beta) deposition (mainly of the C-terminal A beta1-42 form) within the neurones and at the synaptic regions, in the early stages
of the process.
These deposits subsequently appear to give rise to the formation of senile plaques of the diffuse (non-beta-sheet) subtype, which tend to develop spontaneously but rarely proceed to form neuritic plaques.
Additional features accompanying neurodegeneration include accumulations of the `aging pigment,` lipofuscin, intraneuronal changes in the cytoskeleton, vascular changes in the cerebrum, cortical cerebral atrophy, enlargement of the ventricles and increased concentration of oxidative stress markers, many of which are perceived as cardinal features of extensive dysfunction in the protein turnover network. The involvement of ubiquitin is discrete but consistent in many of these molecular structures and seems to account for some critical aspects of the associated neuropathology. Irrespective of these, though, the degenerated canine brain seems to be devoid of
neurofibrillary tangle formation, a manifestation commonly observed in the brain of both aged (cognitively normal) and Alzheimer-affected human subjects.
The fact that canines exhibit clear symptoms of an age-related cognitive decline pertains to the concept of A beta playing a central role in age-related cognitive dysfunction and neurodegeneration.
Source: Dimakopoulos AC, Mayer RJ (2002): Aspects of neurodegeneration in the canine brain. In:
J Nutr 2002 Jun;132(6 Suppl 2):1579S-82S
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