Gamma oscillations and application of 40‐Hz audiovisual stimulation to improve brain function

Chen, Xixi; Shi, Xiaolong; Wu, Yuwei; Zhou, Zhiqing; Chen, Songmei; Han, Yan; Shan, Chunlei

doi:10.1002/brb3.2811

Cited by 13 publications

(8 citation statements)

References 112 publications

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“…An extensive body of prior work has investigated the effects of flicker in response to 1hr of stimulation. Prior studies have shown that 40Hz flicker has multiple effects, including reducing amyloid beta levels, altering microglia and astrocyte morphology, increasing glymphatic clearance, and more (6)(7)(8)(9)17). These prior studies primarily focused on the effects of 1hr of 40Hz flicker or repeated exposures to 1hr of 40Hz flicker.…”

Section: Discussionmentioning

confidence: 99%

“…To do so, we exposed the 5xFAD amyloidosis mouse model to a range of flicker frequencies (constant light, 10Hz, 20Hz, 40Hz) for durations of 30min, 1hr, or 4hr, then used bulk RNA sequencing (RNAseq) to profile transcriptional changes in the visual cortex (VC) and hippocampus (HIP). We used combined audiovisual stimulation for this study because multimodal stimulation is hypothesized to affect more brain regions and prior studies report this stimulation modulates neural activity and AD pathology in the hippocampus (14, 17). We used weighted gene co-expression network analysis (WGCNA) (18) to identify modules of highly correlated co-expressed genes ( Methods ).…”

Section: Introductionmentioning

confidence: 99%

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Frequency and duration of sensory flicker controls astrocyte and neuron specific transcriptional profiles in 5xFAD mice

Bitarafan,

Pybus,

Rivera Moctezuma

et al. 2024

Preprint

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Background: Current clinical trials are investigating gamma frequency sensory stimulation as a potential therapeutic strategy for Alzheimer's disease, yet we lack a comprehensive picture of the effects of this stimulation on multiple aspects of brain function. While most prior research has focused on gamma frequency sensory stimulation, we previously showed that exposing mice to visual flickering stimulation increased MAPK and NFκB signaling in the visual cortex in a manner dependent on duration and frequency of sensory stimulation exposure. Because these pathways control multiple neuronal and glial functions and are differentially activated based on the duration and frequency of flicker stimulation, we aimed to define the transcriptional effects of different frequencies and durations of flicker stimulation on multiple brain functions. Methods: We exposed 5xFAD mice to different frequencies of audio/visual flicker stimulation (constant light, 10Hz, 20Hz, 40Hz) for durations of 0.5hr, 1hr, or 4hr, then used bulk RNAseq to profile transcriptional changes within the visual cortex and hippocampus tissues. Using weighted gene co-expression network analysis, we identified modules of co-expressed genes controlled by frequency and/or duration of stimulation. Results: Within the visual cortex, we found that all stimulation frequencies caused fast activation of a module of immune genes within 1hr and slower suppression of synaptic genes after 4hrs of stimulation. Interestingly, all frequencies of stimulation led to slow suppression of astrocyte specific gene sets, while activation of neuronal gene sets was frequency and duration specific. In contrast, in the hippocampus, immune and synaptic modules were suppressed based on the frequency of stimulation. Specifically,10Hz activated a module of genes associated with mitochondrial function, metabolism, and synaptic translation while 10Hz rapidly suppressed a module of genes linked to neurotransmitter activity. Conclusion: Collectively, our data indicate that the frequency and duration of flicker stimulation controls immune, neuronal, and metabolic genes in multiple regions of the brain affected by Alzheimer's disease. Flicker stimulation may thus represent a potential therapeutic strategy that can be tuned based on the brain region and the specific cellular process to be modulated.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Frequency and duration of sensory flicker controls astrocyte and neuron specific transcriptional profiles in 5xFAD mice

Bitarafan,

Pybus,

Rivera Moctezuma

et al. 2024

Preprint

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“…Importantly, there have also been reports where gamma power (Tülay et al., 2020) or coherence (Stam et al., 2002) remained unaffected in AD patients when compared with healthy controls. Finally, the relationship between gamma oscillations and AD has recently gained increased interest, particularly regarding the potential therapeutic benefits of entraining cortical activity to auditory, visual and somatosensory gamma rhythmic stimuli (Parciauskaite et al., 2021; Traikapi & Konstantinou, 2021; Chen, Shi et al., 2022; Manippa et al., 2022; Nissim et al., 2023). However, as mentioned above, this relationship is far from well‐established (Soula et al., 2023).…”

Section: Introductionmentioning

confidence: 99%

Rodents’ visual gamma as a biomarker of pathological neural conditions

Meneghetti,

Vannini,

Mazzoni

2024

The Journal of Physiology

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Neural gamma oscillations (indicatively 30–100 Hz) are ubiquitous: they are associated with a broad range of functions in multiple cortical areas and across many animal species. Experimental and computational works established gamma rhythms as a global emergent property of neuronal networks generated by the balanced and coordinated interaction of excitation and inhibition. Coherently, gamma activity is strongly influenced by the alterations of synaptic dynamics which are often associated with pathological neural dysfunctions. We argue therefore that these oscillations are an optimal biomarker for probing the mechanism of cortical dysfunctions. Gamma oscillations are also highly sensitive to external stimuli in sensory cortices, especially the primary visual cortex (V1), where the stimulus dependence of gamma oscillations has been thoroughly investigated. Gamma manipulation by visual stimuli tuning is particularly easy in rodents, which have become a standard animal model for investigating the effects of network alterations on gamma oscillations. Overall, gamma in the rodents’ visual cortex offers an accessible probe on dysfunctional information processing in pathological conditions. Beyond vision‐related dysfunctions, alterations of gamma oscillations in rodents were indeed also reported in neural deficits such as migraine, epilepsy and neurodegenerative or neuropsychiatric conditions such as Alzheimer's, schizophrenia and autism spectrum disorders. Altogether, the connections between visual cortical gamma activity and physio‐pathological conditions in rodent models underscore the potential of gamma oscillations as markers of neuronal (dys)functioning. image

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“…Agents that directly pharmacologically target major neuropathological hallmarks of the disease including beta-amyloid (Aß) plaques, taucontaining neurofibrillary tangles and neuroinflammation are the main focus of attention (Cummings et al, 2022;van Dyck et al, 2023). In addition, the therapeutic potential of non-pharmacological approaches, including those targeting brain network dysfunction, is gaining considerable traction (Chen et al, 2022;Manippa et al, 2022). Abnormal brain network activity in patients with AD include a marked reduction in gamma band electroencephalogram oscillations (g, 30-100 Hz) (Casula et al, 2022) a feature that also has been observed in many animal models (Driver et al, 2007;Iaccarino et al, 2016;Bazzigaluppi et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Gamma-patterned sensory stimulation reverses synaptic plasticity deficits in rat models of early Alzheimer's disease

Yin

Ondrejčák

et al. 2023

Preprint

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Non-invasive sensory stimulation in the range of the brain’s gamma rhythm (30-100 Hz) is emerging as a new potential therapeutic strategy for the treatment of Alzheimer’s disease (AD). Here we investigated the effect of repeated combined exposure to 40 Hz synchronized sound and light stimuli on hippocampal long-term potentiation (LTP) in vivo in three rat models of early AD. We employed a very complete model of AD amyloidosis, amyloid precursor protein (APP)-overexpressing transgenic McGill-R-Thy1-APP rats at an early pre-plaque stage, systemic treatment of transgenic APP rats with corticosterone modelling certain environmental AD risk factors and, importantly, intracerebral injection of highly disease-relevant AD patient-derived synaptotoxic beta-amyloid and tau in wild-type animals. We found that daily sessions of 40 Hz sensory stimulation fully abrogated the inhibition of LTP in all three models. Moreover, there was a negative correlation between the magnitude of LTP and the level of active caspase-1 in the hippocampus of transgenic APP animals which suggests that the beneficial effect of 40 Hz stimulation was dependent on modulation of pro-inflammatory mechanisms. Our findings support ongoing clinical trials of gamma-patterned sensory stimulation in early AD.

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Gamma oscillations and application of 40‐Hz audiovisual stimulation to improve brain function

Cited by 13 publications

References 112 publications

Frequency and duration of sensory flicker controls astrocyte and neuron specific transcriptional profiles in 5xFAD mice

Frequency and duration of sensory flicker controls astrocyte and neuron specific transcriptional profiles in 5xFAD mice

Rodents’ visual gamma as a biomarker of pathological neural conditions

Gamma-patterned sensory stimulation reverses synaptic plasticity deficits in rat models of early Alzheimer's disease

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