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

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.

Loss of Caveolin-1 Impairs Light Flicker-Induced Neurovascular Coupling at the Optic Nerve Head

Glaucoma is a neurodegenerative disease, which results in characteristic visual field defects. Intraocular pressure (IOP) remains the main risk factor for this leading cause of blindness. Recent studies suggest that disturbances in neurovascular coupling (NVC) may be associated with glaucoma. The resultant imbalance between vascular perfusion and neuronal stimulation in the eye may precede retinal ganglion cell (RGC) loss and increase the susceptibility of the eye to raised IOP and glaucomatous degeneration. Caveolin-1 (Cav-1) is an integral scaffolding membrane protein found abundantly in retinal glial and vascular tissues, with possible involvement in regulating the neurovascular coupling response. Mutations in Cav-1 have been identified as a major genetic risk factor for glaucoma. Therefore, we aim to evaluate the effects of Cav-1 depletion on neurovascular coupling, retinal vessel characteristics, RGC density and the positive scotopic threshold response (pSTR) in Cav-1 knockout (KO) versus wild type C57/Bl6 mice (WT). Following light flicker stimulation of the retina, Cav-1 KO mice showed a smaller increase in perfusion at the optic nerve head and peripapillary arteries, suggesting defective neurovascular coupling. Evaluation of the superficial capillary plexus in Cav-1 KO mice also revealed significant differences in vascular morphology with higher vessel density, junction density and decreased average vessel length. Cav-1 KO mice exhibited higher IOP and lower pSTR amplitude. However, there was no significant difference in RGC density between Cav-1 KO and wild type mice. These findings highlight the role of Cav-1 in regulating neurovascular coupling and IOP and suggest that the loss of Cav-1 may predispose to vascular dysfunction and decreased RGC signaling in the absence of structural loss. Current treatment for glaucoma relies heavily on IOP-lowering drugs, however, there is an immense potential for new therapeutic strategies that increase Cav-1 expression or augment its downstream signaling in order to avert vascular dysfunction and glaucomatous change.

Assessing horseshoe crab avoidance response of flicker and continuous red-light LED: Gillnets bycatch mitigation

The horseshoe crab has the important roles as macrobenthos, but it is unfriendly for gillnets fisheries because it can damage the fishing net. The horseshoe crab is an ancient, rare, and protected animal so that the fishermen unable to utilize it, so the effort like mitigations need to be conducted like using red light LED. To avoid the learning behavior of horseshoe crab, so that the technology used is red light LED continuous then the red light led with flicker is used as a comparison. This study aims to determine the right type of red-light LED for horseshoe crab bycatch mitigation by the response pattern. The method used was a laboratory experiment. There are 20 adult horseshoe crabs used. The analysis used was descriptively comparative. The results showed that the red-light LED with flicker was most avoided by horseshoe crabs, which is 75%, while the fastest response of horseshoe crab in avoiding light was found in the light with a flicker effect of 22.97 seconds. Based on the horseshoe crab’s response, it can be concluded that the red LED light flicker is better than the red LED continuous as an alternative technology for the mitigation of horseshoe crab bycatch.

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

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.

Evaluation of Flicker of Light Generated by Arc Furnaces

Due to the dynamic nature of load changes, arc devices are receivers that generate disturbances to the network that affect the power quality. The main disturbance generated by these receivers are voltage fluctuations. One of the effects of voltage fluctuations is the flicker of light caused by lighting receivers. The article presents an analysis of changes indicators flicker of light measured in networks supplying arc furnaces. The propagation of voltage fluctuations to the lines supplying lighting receivers was analyzed. The network parameters influencing the amount of light flicker were estimated. The paper presents a method for calculating the increased flicker of light when several electric arc furnaces are operated in parallel. The conclusions regarding the use of the presented research in practical applications are given in the summary.

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

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.