The original models for AD attempted to mimic the neurochemical deficits, mainly in the cholinergic pathways. With a better understanding of the neuropatholog-ical lesions at a molecular level, transgenic models were devised that recapitulated a surprising degree of AD pathology. These include reasonably faithful age dependence, brain region specificity, and appropriate behavioral effects. There is evidence of neuroinflammation in microglial activation, even though many of the mouse strains are deficient in the inflammatory response (Schwab et al., 2004). There is also evidence of oxidative stress, and some of the neurochemical changes are similar to those in AD. Some of the behavioral changes in the ^APP overexpressing mice also resemble facets of early AD dementia.
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