Auditory evoked potentials might have the potential to serve as early indicators related to amyloid beta peptide toxicity.

ABSTRACT

PURPOSE: Accumulation of amyloid beta (Aß) is thought to be the major cause of the development and progression of Alzheimer's disease (AD). The aim of this study is to elucidate the effects of Aß1-42 at increasing concentrations on auditory evoked potentials (AEPs) and to determine possible changes relevant to the accumulation of Aß1-42. MATERIALS AND METHODS: In this study, rats were randomized to following groups (n = 10 per group) sham (0.9% NaCl), Aß-1 (1 µg/µl), Aß-2 (2 µg/µl), Aß-3 (3 µg/µl), Aß-4 (4 µg/µl), Aß-5 (6 µg/µl), Aß-6 (8 µg/µl) and Aß-7 (10 µg/µl) groups obtained by injection of 5 µl per ventricle. Then, AEPs were recorded in freely-moving rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to auditory stimulus. Furthermore, Aß1-42 levels were determined in the temporal cortex. RESULTS: Aß1-42 levels were significantly higher in the temporal cortex in Aß groups compared to the sham. In frontal and parietal regions, P1N1 amplitudes were significantly decreased in Aß-3, 4, 5 and 6 groups, and N1P2 amplitudes were significantly decreased in all Aß groups, whereas in temporal regions, P1N1 and N1P2 amplitudes were decreased in Aß-2,3,4,5,6 and 7 compared to the sham. In the evoked gamma power and phase synchronization of gamma responses, we detected significant decrease after Aß-4 group, whereas a significant decrease in the filtered gamma responses was observed in Aß groups compared to the sham. CONCLUSIONS: AEPs might be used as a biomarker to determine the Aß1-42 related neuronal degeneration in the auditory networks.