ArticleResearch square2026
High-frequency oscillations arise through distinct mechanisms in models of α- synucleinopathy and channelopathy-induced epilepsy.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pathological high-frequency oscillations (HFOs), widely researched in epilepsy, are increasingly being investigated as potential biomarkers of network hyperexcitability in neurodegenerative disorders. This interest is driven by growing evidence of comorbidity between epilepsy and neurodegenerative diseases, particularly Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), suggesting that these HFOs could be useful biomarkers in these disorders. Patients with AD and mouse models of AD exhibit elevated HFOs during neurophysiology recordings, but whether HFOs occur in DLB remains unknown. Methods: To address this question, we quantified cortical HFOs within the spectral range of 250-500 Hz and interictal spikes using surface electroencephalography recordings in a transgenic model of α-synucleinopathy that exhibits features of DLB (A53T mice) and a model of channelopathy-induced epilepsy ( Results: Both A53T and Conclusions: Our findings indicate that HFOs likely arise from different neuronal populations and are generated through distinct mechanisms in these two models. Importantly, this work shows that HFOs are an electroencephalographic abnormality in a model of DLB and supports their potential as a new biomarker for neurodegenerative disorders.
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