Transgenic mice carrying human APPswe and PS1-A264E transgenes (A/P mice) have elevated levels of the highly fibrillogenic amyloid Aβ1-42 (Aβ) and develop amyloid plaques around the age of 9 months. Our aim was to find whether the gradual accumulation of Aβ in these mice can be detected with long-term recording of auditory-evoked potentials. The A/P double-mutant mice had impaired auditory gating and a tendency toward increased latency of the cortical N35 response, but these changes were not age-dependent between 7 and 11 months of age. In a control experiment that included also APP and PS1 single-mutant mice, the A/P double-mutant mice had weaker auditory gating than either APP or PS1 mice. In contrast, increased N35 latency was found in both A/P and APP mice compared with nontransgenic or PS1 mice. The Aβ40 and Aβ42 levels were robustly increased in A/P mice and Aβ40 moderately increased also in APP mice. Plaques were deposited only in A/P mice. We conclude that the impaired auditory gating is associated with the overproduction Aβ42 but does not reflect its amount. In contrast, increased N35 latency is related to the APP genotype independent of Aβ42 production. © 2003 IBRO. Published by Elsevier Science Ltd. All rights reserved.