scholarly journals Non-invasive 40-Hz Light Flicker Ameliorates Alzheimer’s-Associated Rhythm Disorder via Regulating Central Circadian Clock in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Youli Yao ◽  
Ying Ying ◽  
Qiyu Deng ◽  
Wenjiang Zhang ◽  
Huazhang Zhu ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Non Invasive ◽  
Rhythm Disorder ◽  
Light Flicker ◽  
40 Hz

scholarly journals Rhythmic auditory stimulation rescues cognitive flexibility in mutant mice with impaired gamma synchrony

2021 ◽  
Author(s):  
Jingcheng Shi ◽  
Aarron J Phensy ◽  
Vikaas Singh Sohal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sensory Stimulation ◽  
Auditory Stimulation ◽  
Invasive Treatment ◽  
Non Invasive ◽  
Gamma Frequency ◽  
Gamma Synchrony ◽  
Circuit Function ◽  
40 Hz

Neural synchronization at gamma (~40 Hz) frequencies is believed to contribute to brain function and be deficient in disorders including Alzheimer's disease and schizophrenia. Gamma-frequency sensory stimulation has been proposed as a non-invasive treatment for deficient gamma synchrony and associated cognitive deficits, and has been shown to be effective in mouse models of Alzheimer's disease. However, both the mechanism and applicability of this approach remain unclear. Here we tested this approach using mutant (Dlx5/6+/-) mice which have deficits in gamma synchrony and the ability to learn to shift between rules which use different types of cues to indicate reward locations. 40 Hz auditory stimulation rescues rule shifting in Dlx5/6+/- mice. However, this improvement does not outlast the period of stimulation, and is not associated with normalized gamma synchrony, measured using genetically encoded voltage indicators. These results show how gamma-frequency sensory stimulation may improve behavior without fully restoring normal circuit function.

scholarly journals 40 Hz Light Flicker Alters Human Brain Electroencephalography Microstates and Complexity Implicated in Brain Diseases

2021 ◽  
Vol 15 ◽  
Author(s):  
Yiqi Zhang ◽  
Zhenyu Zhang ◽  
Lei Luo ◽  
Huaiyu Tong ◽  
Fei Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Future Development ◽  
Negative Control ◽  
Brain Diseases ◽  
Control Treatment ◽  
Healthy Human ◽  
Light Flicker ◽  
40 Hz

Previous studies showed that entrainment of light flicker at low gamma frequencies provided neuroprotection in mouse models of Alzheimer’s disease (AD) and stroke. The current study was set to explore the feasibility of using 40 Hz light flicker for human brain stimulation for future development as a tool for brain disease treatment. The effect of 40 Hz low gamma frequency light on a cohort of healthy human brains was examined using 64 channel electroencephalography (EEG), followed by microstate analyses. A random frequency light flicker was used as a negative control treatment. Light flicker at 40 Hz significantly increased the corresponding band power in the O1, Oz, and O3 electrodes covering the occipital areas of both sides of the brain, indicating potent entrainment with 40 Hz light flicker in the visual cortex area. Importantly, the 40 Hz light flicker significantly altered microstate coverage, transition duration, and the Lempel-Ziv complexity (LZC) compared to the rest state. Microstate metrics are known to change in the brains of Alzheimer’s disease, schizophrenia, and stroke patients. The current study laid the foundation for the future development of 40 Hz light flicker as therapeutics for brain diseases.

scholarly journals The Effect of 40-Hz Light Therapy on Amyloid Load in Patients with Prodromal and Clinical Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Rola Ismail ◽  
Allan K. Hansen ◽  
Peter Parbo ◽  
Hans Brændgaard ◽  
Hanne Gottrup ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Short Duration ◽  
Neurodegenerative Disorder ◽  
Light Emitting Diode ◽  
Light Therapy ◽  
Association Cortex ◽  
Amyloid Load ◽  
Light Flicker ◽  
40 Hz

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. AD pathology is characterized by abnormal aggregation of the proteins amyloid-β (Aβ) and hyperphosphorylated tau. No effective disease modifying therapies are currently available. A short-duration intervention with 40 Hz light flicker has been shown to reduce brain Aβ load in transgenic mice. We aimed to test the effect of a similar short-duration 40 Hz light flicker regime in human AD patients. We utilized a Light Emitting Diode (LED) light bulb with a 40 Hz flicker. Six Aβ positive patients received 10 days of light therapy, had 2 hours of daily exposure, and underwent a postintervention PiB PET on day 11. After 10 days of light therapy, no significant decrease of PiB SUVR values was detected in any volumes of interest tested (primary visual cortex, visual association cortex, lateral parietal cortex, precuneus, and posterior cingulate) or in the total motor cortex, and longer treatments may be necessary to induce amyloid removal in humans.

40 Hz Light Flicker Promotes Learning and Memory via Long Term Depression in Wild-Type Mice

2021 ◽  
pp. 1-11
Author(s):  
Tian Tian ◽  
Xin Qin ◽  
Yali Wang ◽  
Yan Shi ◽  
Xin Yang
Keyword(s):  
Neural Networks ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Visual Stimulation ◽  
Place Cell ◽  
Wild Type ◽  
Long Term Depression ◽  
Light Flicker ◽  
40 Hz

Background: 40 Hz light flicker is a well-known non-invasive treatment that is thought to be effective in treating Alzheimer’s disease. However, the effects of 40 Hz visual stimulation on neural networks, synaptic plasticity, and learning and memory in wild-type animals remain unclear. Objective: We aimed to explore the impact of 40 Hz visual stimulation on synaptic plasticity, place cell, and learning and memory in wild-type mice. Methods: c-Fos+ cell distribution and in vivo electrophysiology was used to explore the effects of 40 Hz chronic visual stimulation on neural networks and neuroplasticity in wild-type mice. The character of c-Fos+ distribution in the brain and the changes of corticosterone levels in the blood were used to investigate the state of animal. Place cell analysis and novel location test were utilized to examine the effects of 40 Hz chronic visual stimulation on learning and memory in wild-type mice. Results: We found that 40 Hz light flicker significantly affected many brain regions that are related to stress. Also, 40 Hz induced gamma enrichment within 15 min after light flickers and impaired the expression of long-term potentiation (LTP), while facilitated the expression of long-term depression (LTD) in the hippocampal CA1. Furthermore, 40 Hz light flicker enhanced the expression of corticosterone, rendered well-formed place cells unstable and improved animal’s learning and memory in novel local recognition test, which could be blocked by pre-treatment with the LTD specific blocker Glu2A-3Y. Conclusion: These finding suggested that 40 Hz chronic light flicker contains stress effects, promoting learning and memory in wild-type mice via LTD.

Aerobic exercise during exposure to 40Hz light flicker protects against early cognitive impairments in Alzheimer’s disease of 3xTg mice

2020 ◽  
Author(s):  
Sang-Seo Park ◽  
Hye-Sang Park ◽  
Chang-Ju Kim ◽  
Seung-Soo Baek ◽  
Tae-Woon Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Expression ◽  
Cognitive Decline ◽  
Mitochondrial Function ◽  
Early Stage ◽  
Synaptic Function ◽  
Control Group ◽  
Light Flicker ◽  
40 Hz

Abstract Background: Alzheimer’s disease (AD) is a progressive degenerative brain disease and the primary cause of dementia. At an early stage, AD is generally characterized by memory impairment involving recent experiences owing to dysfunctions of the cortex and hippocampus. The lesion gradually spreads to the association cortex. Early amyloid-β (Aβ) deposition and tau protein expression result in a loss of synaptic function, mitochondrial damage, and increased cell death via microglia and astrocyte activation, which ultimately lead to cognitive decline. Exercise has been identified as a powerful tool for preventing AD-related neuroinflammation and cognitive decline, and light flickering at 40 Hz light flicker is known to stabilize gamma oscillations and reduce Aβ. Therefore, we investigated whether exercise under 40-Hz light flickering protects against cognitive decline based on analyses of neuroinflammation, mitochondrial function, and neuroplasticity in the hippocampus in a 3xTg AD mouse model.Methods: Using a 3xTg-AD model, 5-month-old mice were subjected to 12 weeks of exercise treatment and 40-Hz light flickering independently and in combination. Various factors, including spatial learning and memory, long-term memory, hippocampal Aβ, tau, neuroinflammation, pro-inflammatory cytokine expression, mitochondrial function, and neuroplasticity, were analyzed.Results: Aβ and tau proteins levels were significantly reduced in the early stage of AD, resulting in protection against cognitive decline by reduced neuroinflammation and pro-inflammatory cytokines, improved mitochondrial function, reduced apoptosis, and increased synapse-related protein expression. In particular, exercise under 40-Hz light flickering was more effective than exercise or 40-Hz light flickering alone, resulting in improvements in parameter values to levels in the non-transgenic aged-match control group.Conclusions: In this study, exercise under a special environment, such as 40-Hz light flickering, may exert a protective effect against cognitive decline. We detected synergistic effects of exercise and 40-Hz light flickering on pathological changes in the hippocampus in the early cognitive impairment of AD.

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