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 Functional segmentation of the hippocampus in the healthy human brain and in Alzheimer's disease

NeuroImage ◽  
2013 ◽  
Vol 66 ◽  
pp. 28-35 ◽  
Author(s):  
Mojtaba Zarei ◽  
Christian F. Beckmann ◽  
Maja A.A. Binnewijzend ◽  
Menno M. Schoonheim ◽  
Mohammad Ali Oghabian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Healthy Human

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.

Corrigendum to “Functional segmentation of the hippocampus in the healthy human brain and in Alzheimer's disease” [Neuroimage 66 (2013) 28–35]

NeuroImage ◽  
2013 ◽  
Vol 83 ◽  
pp. 1109
Author(s):  
Mojtaba Zarei ◽  
Christian F. Beckmann ◽  
Maja A.A. Binnewijzend ◽  
Menno M. Schoonheim ◽  
Mohammad Ali Oghabian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Healthy Human

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.

Small RNA sequencing revealed dysregulated piRNAs in Alzheimer's disease and their probable role in pathogenesis

2017 ◽  
Vol 13 (3) ◽  
pp. 565-576 ◽  
Author(s):  
Jyoti Roy ◽  
Arijita Sarkar ◽  
Sibun Parida ◽  
Zhumur Ghosh ◽  
Bibekanand Mallick
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Rna Sequencing ◽  
Small Rna ◽  
Small Rna Sequencing ◽  
Healthy Human ◽  
Probable Role ◽  
First Time

For the first time, this study reports specific piRNA signatures in a healthy human brain and an AD-diagnosed brain and decrypted the regulatory roles of dysregulated piRNAs in the pathogenesis of AD.

Phenylalanine Metabolism is Dysregulated in Human Hippocampus with Alzheimer’s Disease Related Pathological Changes

2021 ◽  
pp. 1-14
Author(s):  
Pan Liu ◽  
Qian Yang ◽  
Ning Yu ◽  
Yan Cao ◽  
Xue Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Pathological Examination ◽  
Pathological Changes ◽  
Targeted Metabolomics ◽  
Phenylpyruvic Acid ◽  
Postmortem Human Brain ◽  
Metabolic Dysregulation ◽  
Phenylalanine Metabolism

Background: Alzheimer’s disease (AD) is one of the most challenging diseases causing an increasing burden worldwide. Although the neuropathologic diagnosis of AD has been established for many years, the metabolic changes in neuropathologic diagnosed AD samples have not been fully investigated. Objective: To elucidate the potential metabolism dysregulation in the postmortem human brain samples assessed by AD related pathological examination. Methods: We performed untargeted and targeted metabolomics in 44 postmortem human brain tissues. The metabolic differences in the hippocampus between AD group and control (NC) group were compared. Results: The results show that a pervasive metabolic dysregulation including phenylalanine metabolism, valine, leucine, and isoleucine biosynthesis, biotin metabolism, and purine metabolism are associated with AD pathology. Targeted metabolomics reveal that phenylalanine, phenylpyruvic acid, and N-acetyl-L-phenylalanine are upregulated in AD samples. In addition, the enzyme IL-4I1 catalyzing transformation from phenylalanine to phenylpyruvic acid is also upregulated in AD samples. Conclusion: There is a pervasive metabolic dysregulation in hippocampus with AD-related pathological changes. Our study suggests that the dysregulation of phenylalanine metabolism in hippocampus may be an important pathogenesis for AD pathology formation.

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