In humans, abnormal hyperphosphorylation of the micro-tubule protein tau leads to the development of neuro-fibrillary tangles (NFTs), which are linked to cognitive decline in aging (Duyckaerts et al., 1997). In the dog, the role of neurofibrillary tangle formation is unclear. Although dogs exhibit early stages of tangle formation characterized by tau phosphorylation and an intracellular punctuate distribution, the morphology is distinct from the human brain and does not progress into thioflavine-S or silver positive NFTs (Cummings et al., 1996). Using AT8, a marker for early neurofibrillary tangle formation, Head et al. (2001) observed hyperphosphorylated tau in select neuronal populations in middle-aged but not old dogs. This is consistent with earlier studies of cytoskeletal abnormalities (Cumming et al., 1996), distended neurites (Wisniewski et al., 1970), and tau positive neurons (Uchida et al., 1993) in the dog.
One explanation for the absence of NFTs in the dog is that the tau protein in the dog is different from human tau protein and thus dogs are not predisposed to develop full NFTs with age (Head et al., 2001). The implication of this finding is that beta-amyloid and not tau pathology may be sufficient to lead to cognitive and behavioral dysfunction in the aging dog. In the absence of NFTs, cognitive dysfunction increases proportionately with beta-amyloid deposition in the dog. All old dogs develop pathology, but old animals with extensive beta-amyloid deposition are more impaired than those with less beta-amyloid deposition (Head et al., 1998). This suggests that beta-amyloid deposition may influence neuronal function and may lead to impaired cognition.
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