Gamma Entrainment Improves Synchronization Deficits in Dementia Patients

Abstract

Non-invasive gamma entrainment has shown promising results in alleviating cognitive symptoms of Alzheimer's disease in mice and humans. In this study, we examine improvements in the synchronization characteristics of the brain's oscillations induced by 40Hz auditory stimulation based on electroencephalography data recorded from a group of dementia patients. We observed that when the quality of entrainment surpasses a certain level, several indicators of brain synchronization significantly improve. Specifically, the entrained oscillatory activity maintains temporal phase stability in the frontal, parietal, and occipital regions, and persistent spatial phase coupling between them. In addition, notable theta-gamma phase-amplitude coupling is observed in these areas. Interestingly, a high theta power at rest predicts the quality of entrainment. We identify differentiating attributes of temporal/spatial synchronization and cross-frequency coupling in the data of two groups with entrained and non-entrained responses which point to enhanced network synchronization caused by entrainment and can explain its potential therapeutic effects.

Auditory gamma-band entrainment enhances default mode network connectivity in dementia patients

“…While stimulating the brain with 40 Hz auditory or visual stimuli is referred to as entrainment, our results show that such stimulation does not necessarily cause notable entrained oscillatory activity in all brains. Based on earlier studies on entrainment 26,37,50 , a clear response of the brain to the stimulant frequency is expected as a peak in the spectrogram of the recorded response on that frequency. In Fig.…”

“…It is still a matter of debate whether network alterations such as deficits in gamma activity are a consequence of the underlying neurodegenerative processes or they indeed play a causal role in inducing neuropathological changes that promote the disease progression. While neuropathological effects such as the aggregation of surplus Aβ in intercellular space and the ensuing synaptic loss are reported to cause hyperexcitability in excitatory neural populations leading to network disruption 1,8 , other evidences point to the presence of network alterations such as reduced gamma oscillations, decreased cross-frequency coupling activity, and diminished functional connectivity in the default mode network (DMN) even before plaque aggregates are ostensibly detectable [20][21][22][23][24][25][26] . The DMN is one of the most vulnerable networks affected by Aβ deposits in the early stages of the disease [27][28][29] .…”

“…Interventions based on stimulating neural populations in the gamma band have been recently proposed and are under examination on animal models of AD 20,[33][34][35] and in human studies 26,[36][37][38][39][40][41][42][43][44] . These approaches aim to reinvigorate the functionality of the brain networks through synchronized pumping of rhythmic energy via one or multiple sensory modalities.…”