In recent years, the generation of many types of transgenic mice, including those over-expressing amyloid precursor protein (APP), have brought mice to the forefront of aging research since they present extensive Aβ deposition and can be considered an animal model of AD. Dean et al44 studied age-related behavioral differences in the C57BL mouse and observed that, in the passive avoidance test, the number of mice failing to avoid the dark chamber in which the mice had previously been shocked is higher at 9 than at 3 months of age. Similarly, 10-month-old mice need a higher Inhibitors,research,lifescience,medical number of trials to criterion in a T-maze task than the 3-month-old mice. The cognitive impairment revealed by these tests

becomes progressively more severe at 23 and 31 months of age. Impairment in the acquisition and retention of the water maze task was detected in 18- to 19-month-old C57BL mice and was associated with a decrease in the volume of the septal cholinergic neurons.45 It has already been mentioned that MCI can be considered Inhibitors,research,lifescience,medical to be a transitional state between normal aging and dementia. Since transgenic mice presenting Aβ deposits are considered

to be a model of AD, it should be possible to detect a prodromal Inhibitors,research,lifescience,medical phase of the disease with the features of MCI. The learning deficit related to age and Aβ plaques was investigated by Chen et al46 in PDAPP transgenic mice and nontransgenic mice of different ages. Age did not affect the object recognition test in transgenic or wild-type mice. Conversely, in the Morris maze Inhibitors,research,lifescience,medical test, an age-related impairment of spatial memory was evident in both groups of mice, but was clearly more profound in the transgenic mice, and a relationship was

found between the Aβ plaque burden and learning impairment. However, only in the group of young (9 months) transgenic mice was it possible to detect an impairment in Inhibitors,research,lifescience,medical learning the first platform location that was associated with a minimal plaque burden and could reasonably be considered as MCI. Retardation in initial learning and in learning CYTH4 a new escape location had also been previously observed47 in transgenic mice for APP695 in which no amyloid deposition was detected. In contrast to these results, Westerman et al48 demonstrated that, in Tg 2576 mice overexpressing human APP695 with the “Swedish” mutation, spatial memory impairment, evaluated in the Morris water maze, could be detected beginning from the age of 6 to 11 months and coincided with the appearance of the insoluble form of Aβ. In testing a similar strain in a passive avoidance task, it was demonstrated49 that, in the transgenic mice, memory impairment appeared at about 8 months of age and progressed with aging. At 8 months, there were few www.selleckchem.com/products/Trichostatin-A.html senile plaques and an initial decrease in ACh content in several brain regions including the cortex and the hippocampus.