Alzheimer’s disease (AD) is characterized by the development of learning and memory deficits. Particularly at later states of the disease, patients also progressively exhibit cognitive impairments and deficits in central sensory processing. Accumulation of amyloid-β in the brain of patients is thought to play a direct role in the initiation of AD. We use double transgenic APP23 x PS45 mice, who overexpress both β-amyloid precursor protein and mutant presenilin 1 under the control of Thy-1 promoter as a model system to study the consequences of enhanced β-amyloid levels. With two-photon based fluorometric calcium imaging we detected age-dependent impairments of both spontaneous and stimulus evoked neuronal activity on the level of individual neurons. In addition we also found dramatic changes in the longrange coherence of wave-like calcium transients with CCDcamera based calcium imaging. These transients reflect synchronous activity of populations of neurons and are involved in the coordination of brain networks. Phenotypical analysis of mutant mice showed age-dependent impairments in spatial and working memory tasks as well as in a test for visual acuity. These findings indicate a correlation between changes in the neuronal activity and the behavior.
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