Sensorimotor deficits have been described in several neuropsychiatric disorders including Alzheimer's disease. The aim of the present study was to evaluate possible sensorimotor gating deficits in the Tg4-42 mouse model of Alzheimer's disease using the prepulse inhibition task (PPI). Previous studies indicated that the hippocampus is essentially involved in the regulation of PPI. We analyzed 7-month-old homozygous Tg4-42 mice as mice at this age display severe neuron loss especially in the CA1 region of the hippocampus. Our results revealed a reduced startle response and PPI in Tg4-42 mice. The observed deficits in startle response and PPI are likely due to altered sensory processing abilities rather than hearing deficits as Tg4-42 displayed intact hearing in the fear conditioning task. The present study demonstrates for the first time that sensorimotor gating is impaired in Tg4-42 mice. Analyzing startle response as well as the PPI may offer valuable measurements to assess the efficacy of therapeutic strategies in the future in this Alzheimer's disease model.
Keywords: Alzheimer’s disease; N-terminally truncated Aβ; cognitive deficits; fear conditioning; hippocampus; neuron loss; prepulse inhibition; sensorimotor gating.
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