Conclusions
Olfactory impairments and spatial learning deficits were shown at the same early age in the Tg6799 mice. Thus the olfactory deficits do not precede other behavioral symptoms, according to the data obtained. Histological data implicates that soluble amyloid-β rather than plaques is responsible for the first behavioral symptoms.
To determine the value of the Tg6799 strain to research on human AD more research is needed, but results are promising and the strain is suitable for research on olfactory impairment
Implications
Research on the development of behavioral symptoms in AD model mice is necessary to determine the value of the models to research on human AD. Symptoms of human AD presents in a highly specific order and to determine how comparable the mouse models are to humans with AD.
Research on olfactory impairment in these mice might also lead to valuable insights in
determining the pattern of AD neuropathology development. The symptoms of AD arise in a progressive pattern but it is not understood how or why this symptomatic timeline is so consistent between cases and individuals. One hypothesis is that the neuropathologies of AD spread in a predetermined pattern and that the symptoms and the order in which they arise are effects of this pattern. Another hypothesis is that the neuropathological changes spread and progress evenly throughout the brain and it is due to differences in susceptibility to these pathologies that different symptoms arise at different times. In other words; the systems that are most vulnerable to the effects of the developed neuropathologies are affected first. In this context, studying the olfactory impairments that arise in AD can lead to valuable insights.
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Last updated:
05/18/10