Age-related modifications of electroencephalogram coherence in mice models of Alzheimer’s disease and amyotrophic lateral sclerosis

Vorobyov, Vasily, Deev, Alexander, Chaprov, Kirill, Ustyugov, Aleksey A. ORCID: https://orcid.org/0000-0003-1977-4797 and Lysikova, Ekaterina 2023. Age-related modifications of electroencephalogram coherence in mice models of Alzheimer’s disease and amyotrophic lateral sclerosis. Biomedicines 11 (4) , 1151. 10.3390/biomedicines11041151

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Abstract

Evident similarities in pathological features in aging and Alzheimer’s disease (AD) raise the question of a role for natural age-related adaptive mechanisms in the prevention/elimination of disturbances in interrelations between different brain areas. In our previous electroencephalogram (EEG) studies on 5xFAD- and FUS-transgenic mice, as models of AD and amyotrophic lateral sclerosis (ALS), this suggestion was indirectly confirmed. In the current study, age-related changes in direct EEG synchrony/coherence between the brain structures were evaluated. Methods: In 5xFAD mice of 6-, 9-, 12-, and 18-month ages and their wild-type (WT5xFAD) littermates, we analyzed baseline EEG coherence between the cortex, hippocampus/putamen, ventral tegmental area, and substantia nigra. Additionally, EEG coherence between the cortex and putamen was analyzed in 2- and 5-month-old FUS mice. Results: In the 5xFAD mice, suppressed levels of inter-structural coherence vs. those in WT5xFAD littermates were observed at ages of 6, 9, and 12 months. In 18-month-old 5xFAD mice, only the hippocampus ventral tegmental area coherence was significantly reduced. In 2-month-old FUS vs. WTFUS mice, the cortex–putamen coherence suppression, dominated in the right hemisphere, was observed. In 5-month-old mice, EEG coherence was maximal in both groups. Conclusion: Neurodegenerative pathologies are accompanied by the significant attenuation of intracerebral EEG coherence. Our data are supportive for the involvement of age-related adaptive mechanisms in intracerebral disturbances produced by neurodegeneration.

Item Type:	Article
Date Type:	Published Online
Status:	Published
Schools:	Medicine Biosciences
Additional Information:	License information from Publisher: LICENSE 1: URL: https://creativecommons.org/licenses/by/4.0/, Type: open-access
Publisher:	MDPI
ISSN:	2227-9059
Date of First Compliant Deposit:	9 May 2023
Date of Acceptance:	9 April 2023
Last Modified:	30 Jul 2024 13:33
URI:	https://orca.cardiff.ac.uk/id/eprint/159318

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