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

Abstract Purpose Accumulation of amyloid beta (Aβ) 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 Aβ1-42 at increasing concentrations on auditory evoked potentials (AEPs) and to determine possible changes relevant to the accumulation of Aβ1-42. Materials and methods In this study, rats were randomized to following groups (n = 10 per group): sham (0.9% NaCl), Aβ-1 (1 μg/μl), Aβ-2 (2 μg/μl), Aβ-3 (3 μg/μl), Aβ-4 (4 μg/μl), Aβ-5 (6 μg/μl), Aβ-6 (8 μg/μl) and Aβ-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, Aβ1-42 levels were determined in the temporal cortex. Results Aβ1-42 levels were significantly higher in the temporal cortex in Aβ groups compared to the sham. In frontal and parietal regions, P1N1 amplitudes were significantly decreased in Aβ-3, 4, 5 and 6 groups, and N1P2 amplitudes were significantly decreased in all Aβ groups, whereas in temporal regions, P1N1 and N1P2 amplitudes were decreased in Aβ-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 Aβ-4 group, whereas a significant decrease in the filtered gamma responses was observed in Aβ groups compared to the sham. Conclusions AEPs might be used as a biomarker to determine the Aβ1-42 related neuronal degeneration in the auditory networks.