Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,080 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Showing posts with label 60 Hertz flickering light. Show all posts
Showing posts with label 60 Hertz flickering light. Show all posts
Iaccarino HF, Singer AC, Martorell AJ, Rudenko A, Gao F, Gillingham TZ, Mathys H, Seo J, Kritskiy O, Abdurrob F, Adaikkan C, Canter RG, Rueda R, Brown EN, Boyden ES, Tsai LH.Nature. 2024 Dec;636(8042):E2. doi: 10.1038/s41586-024-08343-7.PMID: 39592835No abstract available.
Abstract
Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer's disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1-40 and Aβ 1-42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ1-40 and Aβ1-42 levels in the visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate Alzheimer's-disease-associated pathology.
Biophoton
therapy is a form of complementary and alternative light therapy that
uses specific wavelengths of light to stimulate the body's natural
self-healing processes
. It is based on the theory that living
cells emit very low levels of light, or "biophotons," which play a role
in cellular communication and regulation.
Yes, biophotons are real; they are extremely faint light particles (ultra-weak photon emissions or UPE) emitted by all living cells as byproducts of metabolic processes, detectable with sensitive equipment but invisible to the naked eye, and research suggests they play roles in cellular communication, signaling, and potentially even health indicators.
James Z Liu1,2*, Helen Y Gu1,2, Mariola Smotrys1, Seth Robinson2, Huixia Yu2, Devin R Liu2, and Sherry Liu1
1First Institute of All Medicines, 139 Pittsburgh Road, Butler, PA 16001, USA
2Tesla Bio Healing, LLC. 111 McCoy Street, Milford, DE 19963, USA
ABSTRACT
Background:
Effective treatments for chronic stroke remain a critical unmet medical need. Conventional rehabilitation approaches often yield limited
functional recovery, especially in patients with long-standing deficits. Emerging evidence suggests that biophoton-based therapies may offer a novel, non
invasive solution to support neuroregeneration.
Objective:
To evaluate the therapeutic efficacy and safety of Automatic Biophoton Generators (ABGs) in patients with chronic stroke using validated clinical,
neurological, and neurophysiological outcome measures.
Methods:
A randomized, triple-blind, placebo-controlled clinical trial was conducted with 46 chronic stroke patients who received either active ABG
treatment (n = 26) or placebo devices (n = 20) over two weeks. Participants in the placebo group were later crossed over to receive active treatment for
an additional four weeks. Each treatment group received therapy with 4 ABGs placed around a hotel bed. Stroke recovery was assessed using the Stroke
Impact Scale (SIS), SF-36 quality-of-life survey, clinician-led neurological examinations, and quantitative Electroencephalography (qEEG) with Event
Related Potentials (ERP). Additional evaluations included 3D Non-Linear Scanning (3D-NLS) for energetic brain imaging and Bio-Well analysis for organ
and meridian energy coherence.
Results:
Biophoton therapy resulted in statistically significant improvements in SIS scores, stroke recovery rate, neurological exam scores, and quality-of
life measures (p < 0.01). qEEG revealed increased posterior alpha frequencies, reduced theta/beta ratios, and improved ERP latencies, indicating enhanced
attention, memory processing, and cognitive speed. 3D-NLS imaging showed rapid cortical reactivation and restored hemispheric balance after only 6
days of therapy. Bio-Well analysis demonstrated systemic energy restoration across the brain, cardiovascular system, and endocrine organs. No adverse
events were reported.
Conclusion:
This study provides strong clinical and neurophysiological evidence that ABG-based biophoton therapy significantly improves functional
outcomes in patients with chronic stroke. The therapy was well tolerated and offers a promising, non-invasive approach to address long-standing neurological
impairments. These findings support the broader potential of biophoton quantum therapy in treating neurodegenerative and chronic inflammatory disorders.
Summary: A long-term study found that daily 40Hz light and sound stimulation may help slow cognitive decline in people with late-onset Alzheimer’s disease. After two years of treatment, participants maintained stronger cognitive performance than typical Alzheimer’s patients and showed reduced levels of tau protein, a key disease biomarker.
The noninvasive therapy, known as GENUS, works by synchronizing brain activity to a 40Hz gamma rhythm through light and sound. While early-onset patients saw fewer benefits, researchers say the results highlight the potential for a safe, at-home intervention to delay Alzheimer’s progression.
Key Facts
Sustained Benefits: Late-onset Alzheimer’s participants maintained higher cognitive scores and improved sleep patterns over two years.
Biomarker Reduction: Two participants showed significant decreases in plasma tau levels, linked to Alzheimer’s pathology.
Safe and Noninvasive: The GENUS 40Hz light-and-sound therapy was well tolerated and feasible for daily home use.
Source: Picower Institute at MIT
A new research paper documents the outcomes of five volunteers who continued to receive 40Hz light and sound stimulation for around two years after participating in an MIT early-stage clinical study of the potential Alzheimer’s disease therapy.
The results show that for the three participants with late-onset Alzheimer’s disease, several measures of cognition remained significantly higher than comparable Alzheimer’s patients in national databases.
Moreover, in the two late-onset volunteers who donated plasma samples, levels of Alzheimer’s biomarker tau proteins were significantly decreased.
The three volunteers who experienced these benefits were all female. The two other participants, each of whom were males with early-onset forms of the disease, did not exhibit significant benefits after two years.
The dataset, while small, represents the longest-term test so far of the safe, non-invasive treatment method (called GENUS, for gamma entrainment using sensory stimuli), which is also being evaluated in a nationwide clinical trial run by MIT-spinoff company Cognito Therapeutics.
“This pilot study assessed the long-term effects of daily 40Hz multimodal GENUS in patients with mild AD,” the authors wrote in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
“We found that daily 40Hz audiovisual stimulation over 2 years is safe, feasible, and may slow cognitive decline and biomarker progression, especially in late-onset AD patients.”
Diane Chan, a former research scientist in The Picower Institute for Learning and Memory and neurologist at Massachusetts General Hospital, is the study’s lead and co-corresponding author. Picower Professor Li-Huei Tsai, director of The Picower Institute and the Aging Brain Initiative at MIT, is the study’s senior and co-corresponding author.
An “open label” extension
In 2020, MIT enrolled 15 volunteers with mild Alzheimer’s disease in an early-stage trial to evaluate whether an hour a day of 40Hz light and sound stimulation, delivered via an LED panel and speaker in their homes, could deliver clinically meaningful benefits.
Several studies in mice had shown that the sensory stimulation increases the power and synchrony of 40Hz gamma frequency brain waves, preserves neurons and their network connections, reduces Alzheimer’s proteins such as amyloid and tau, and sustains learning and memory. Several independent groups have also made similar findings over the years.
MIT’s trial, though cut short by the Covid-19 pandemic, found significant benefits after three months. The new study examines outcomes among five volunteers who continued to use their stimulation devices on an “open label” basis for two years.
These volunteers came back to MIT for a series of tests 30 months after their initial enrollment. Because four participants started the original trial as controls (meaning they initially did not receive 40Hz stimulation), their open label usage was six to 9 months shorter than the 30-month period.
The testing at 0, 3 and 30 months of enrollment included measurements of their brain wave response to the stimulation, MRI scans of brain volume, measures of sleep quality and a series of five standard cognitive and behavioral tests.
Two participants gave blood samples. For comparison to untreated controls, the researchers combed through three national databases of Alzheimer’s patients, matching thousands of them on criteria such as age, gender, initial cognitive scores, and retests at similar timepoints across a 30-month span.
Outcomes and outlook
The three female late-onset Alzheimer’s volunteers showed improvement or slower decline on most of the cognitive tests, including significantly positive differences compared to controls on three of them.
These volunteers also showed increased brain-wave responsiveness to the stimulation at 30 months and showed improvement in measures of circadian rhythms. In the two late-onset volunteers who gave blood samples, there were significant declines in phosphorylated tau (47 percent for one and 19.4 percent for the other) on a test recently approved by the FDA as the first plasma biomarker for diagnosing Alzheimer’s.
“One of the most compelling findings from this study was the significant reduction of plasma pTau217, a biomarker strongly correlated with AD pathology, in the two late-onset patients in whom follow-up blood samples were available,” the authors wrote in the journal.
“These results suggest that GENUS could have direct biological impacts on Alzheimer’s pathology, warranting further mechanistic exploration in larger randomized trials.”
Though the initial trial results showed preservation of brain volume at 3 months among those who received 40Hz stimulation, that was not significant at the 30-month timepoint.
And the two male early-onset volunteers did not show significant improvements on cognitive test scores. Notably, the early onset patients showed significantly reduced brain-wave responsiveness to the stimulation.
Though the sample is small, the authors hypothesize that the difference between the two sets of patients is likely attributable to the difference in disease onset rather than the difference in gender.
“GENUS may be less effective in early onset Alzheimer’s disease patients, potentially owing to broad pathological differences from late-onset Alzheimer’s disease that could contribute to differential responses,” the authors wrote. “Future research should explore predictors of treatment response, such as genetic and pathological markers.”
ease onset rather than the difference in gender.
“GENUS may be less effective in early onset Alzheimer’s disease patients, potentially owing to broad pathological differences from late-onset Alzheimer’s disease that could contribute to differential responses,” the authors wrote. “Future research should explore predictors of treatment response, such as genetic and pathological markers.”
Has your doctor verified that you had myelin damage from your stroke? What protocols are being used to fix such damage?
Your competent? doctor and hospital need to ensure human testing gets done. I already bought a 40 Hertz light, not waiting decades before it is confirmed in humans.
This one mentions a 60 Hertz flickering light so ask your competent? doctor which one is better. No knowledge of either is a fireable offense!
Summary: A new study finds that 40Hz light and sound
therapy helps maintain myelin, a crucial brain structure, in
Alzheimer’s patients. This therapy, which protects neurons and supports
brain function, could offer new treatment avenues for neurodegenerative
diseases.
Researchers discovered that this stimulation enhances
neural connections and reduces harmful inflammation. The therapy also
shows potential for treating other conditions involving myelin loss,
such as multiple sclerosis.
Key Facts:
40Hz sensory stimulation preserves myelin in Alzheimer’s patients.
The therapy enhances neural connections and reduces inflammation.
Potential applications include treatment for multiple sclerosis.
Source: Picower Institute at MIT
Early-stage trials in
Alzheimer’s disease patients and studies in mouse models of the disease
have suggested positive impacts on pathology and symptoms from exposure
to light and sound presented at the “gamma” band frequency of 40 Hz.
A
new study zeroes in on how 40Hz sensory stimulation helps to sustain an
essential process in which the signal-sending branches of neurons,
called axons, are wrapped in a fatty insulation called myelin. Often
called the brain’s “white matter,” myelin protects axons and insures
better electrical signal transmission in brain circuits.
Amorim
and Tsai’s team found that 40Hz light and sound not only preserved
myelination in the brains of cuprizone-exposed mice, it also appeared to
protect oligodendrocytes (the cells that myelinate neural axons),
sustain the electrical performance of neurons, and preserve a key marker
of axon structural integrity. Credit: Neuroscience News
“Previous
publications from our lab have mainly focused on neuronal protection,”
said Li-Huei Tsai, Picower Professor in The Picower Institute for
Learning and Memory and the Department of Brain and Cognitive Sciences
at MIT and senior author of the new study in Nature Communications.
Tsai also lead’s MIT’s Aging Brain Initiative. “But this study shows
that it’s not just the gray matter, but also the white matter that’s
protected by this method.”
This year Cognito Therapeutics, the spin-off company that licensed
MIT’s sensory stimulation technology, published phase II human trial
results in the Journal of Alzheimer’s Disease indicating that 40Hz light and sound stimulation significantly slowed the loss of myelin in volunteers with Alzheimer’s.
Also
this year Tsai’s lab published a study showing that gamma sensory
stimulation helped mice withstand neurological effects of chemotherapy
medicines, including by preserving myelin. In the new study, members of
Tsai’s lab led by former postdoc Daniela Rodrigues Amorim used a common
mouse model of myelin loss—a diet with the chemical cuprizone— to
explore how sensory stimulation preserves myelination.
Amorim and
Tsai’s team found that 40Hz light and sound not only preserved
myelination in the brains of cuprizone-exposed mice, it also appeared to
protect oligodendrocytes (the cells that myelinate neural axons),
sustain the electrical performance of neurons, and preserve a key marker
of axon structural integrity.
When
the team looked into the molecular underpinnings of these benefits,
they found clear signs of specific mechanisms including preservation of
neural circuit connections called synapses; a reduction in a cause of
oligodendrocyte death called “ferroptosis;” reduced inflammation; and an
increase in the ability of microglia brain cells to clean up myelin
damage so that new myelin could be restored.
“Gamma stimulation promotes a healthy environment,” said Amorim who
is now a Marie Curie Fellow at the University of Galway in Ireland.
“There are several ways we are seeing different effects.”
The
findings suggest that gamma sensory stimulation may help not only
Alzheimer’s disease patients but also people battling other diseases
involving myelin loss, such as multiple sclerosis, the authors wrote in
the study.
Maintaining myelin
To conduct
the study, Tsai and Amorim’s team fed some male mice a diet with
cuprizone and gave other male mice a normal diet for six weeks. Halfway
into that period, when cuprizone is known to begin causing its most
acute effects on myelination, they exposed some mice from each group to
gamma sensory stimulation for the remaining three weeks.
In this
way they had four groups: completely unaffected mice, mice that received
no cuprizone but did get gamma stimulation, mice that received
cuprizone and constant (but not 40Hz) light and sound as a control, and
mice that received cuprizone and also gamma stimulation.
After
the six weeks elapsed, the scientists measured signs of myelination
throughout the brains of the mice in each group. Mice that weren’t fed
cuprizone maintained healthy levels, as expected. Mice that were fed
cuprizone and didn’t receive 40Hz gamma sensory stimulation showed
drastic levels of myelin loss.
Cuprizone-fed mice that received 40Hz stimulation retained
significantly more myelin, rivaling the health of mice never fed
cuprizone by some, but not all, measures.
The researchers also
looked at numbers of oligodendrocytes to see if they survived better
with sensory stimulation. Several measures revealed that in mice fed
cuprizone, oligodendrocytes in the corpus callosum region of the brain
(a key point for the transit of neural signals because it connects the
brain’s hemispheres) were markedly reduced. But in mice fed cuprizone
and also treated with gamma stimulation, the number of cells were much
closer to healthy levels.
Electrophysiological tests among neural
axons in the corpus callosum showed that gamma sensory stimulation was
associated with improved electrical performance in cuprizone-fed mice
who received gamma stimulation compared to cuprizone-fed mice left
untreated by 40Hz stimulation.
And when researchers looked in the
anterior cingulate cortex region of the brain, they saw that MAP2, a
protein that signals the structural integrity of axons, was much better
preserved in mice that received cuprizone and gamma stimulation compared
to cuprizone-fed mice who did not.
Molecular mechanisms
A key goal of the study was to identify possible ways in which 40Hz sensory stimulation may protect myelin.
To find out, the researchers conducted a sweeping assessment of
protein expression in each mouse group and identified which proteins
were differentially expressed based on cuprizone diet and exposure to
gamma frequency stimulation. The analysis revealed distinct sets of
effects between the cuprizone mice exposed to control stimulation and
cuprizone-plus-gamma mice.
A highlight of one set of effects was
the increase in MAP2 in gamma-treated cuprizone-fed mice. A highlight of
another set was that cuprizone mice who received control stimulation
showed a substantial deficit in expression of proteins associated with
synapses. The gamma-treated cuprizone-fed mice did not show any
significant loss, mirroring results in a 2019 Alzheimer’s
40Hz study that showed synaptic preservation.
This result is
important, the researchers wrote, because neural circuit activity, which
depends on maintaining synapses, is associated with preserving myelin.
They confirmed the protein expression results by looking directly at
brain tissues.
Another set of protein expression results hinted at
another important mechanism: ferroptosis. This phenomenon, in which
errant metabolism of iron leads to a lethal buildup of reactive oxygen
species in cells, is a known problem for oligodendrocytes in the
cuprizone mouse model.
Among the
signs was an increase in cuprizone-fed, control stimulation mice in
expression of the protein HMGB1, which is a marker of
ferroptosis-associated damage that triggers an inflammatory response.
Gamma stimulation, however, reduced levels of HMGB1.
Looking more deeply at the cellular and molecular response to
cuprizone demyelination and the effects of gamma stimulation, the team
assessed gene expression using single-cell RNA sequencing technology.
They
found that astrocytes and microglia became very inflammatory in
cuprizone-control mice but gamma stimulation calmed that response. Fewer
cells became inflammatory and direct observations of tissue showed that
microglia became more proficient at clearing away myelin debris, a key
step in effecting repairs.
The team also learned more about how
oligodendrocytes in cuprizone-fed mice exposed to 40Hz sensory
stimulation managed to survive better. Expression of protective proteins
such as HSP70 increased and as did expression of GPX4, a master
regulator of processes that constrain ferroptosis.
In addition to
Amorim and Tsai, the paper’s other authors are Lorenzo Bozzelli, TaeHyun
Kim, Liwang Liu, Oliver Gibson, Cheng-Yi Yang, Mitch Murdock, Fabiola
Galiana-Meléndez, Brooke Schatz, Alexis Davison, Md Rezaul Islam, Dong
Shin Park, Ravikiran M. Raju, Fatema Abdurrob, Alissa J. Nelson, Jian
Min Ren, Vicky Yang and Matthew P. Stokes.
Funding: Fundacion
Bancaria la Caixa, The JPB Foundation, The Picower Institute for
Learning and Memory, the Carol and Gene Ludwig Family Foundation, Lester
A. Gimpelson, Eduardo Eurnekian, The Dolby Family, Kathy and Miguel
Octavio, the Marc Haas Foundation, Ben Lenail and Laurie Yoler, and the
National Institutes of Health provided funding for the study.
About this neurology and neuroscience research news
Author: David Orenstein Source: Picower Institute at MIT Contact: David Orenstein – Picower Institute at MIT Image: The image is credited to Neuroscience News
Cognito
Therapeutics is conducting a Phase III trial with more than 500
participants using a drug-free headset for 12 months. The headset's
stimulation can clear diffuse amyloid that may not show up on PET scans.
The CEO believes the device could be used as a standalone therapy or in
combination with Alzheimer's drugs to slow disease progression.Read More
SAN DIEGO — Light exposure and stimulation of the locus coeruleus may
be a promising way to delay Alzheimer’s disease progression, according
to a presenter at the Alzheimer’s Association International Conference.
“With light stimulation we try to target the locus coeruleus (LC),
which has huge implications in earlier stages of Alzheimer’s disease,” Elise Beckers,
of Limburg Alzheimer’s Centre at Maastricht University in the
Netherlands, said during her poster presentation. “We also know the
pupil is somehow linked to LC activity and that would be an easy
readout, since the pupil is more easily accessible compared to the
brain.”
Source: Adobe Stock.
Understanding the role of LC structure and function in the earliest stages of AD neuropathology
and that light exposure may be a promising way to delay disease
progression, Beckers and colleagues sought to characterize pupil
responses to light during fMRI and determine its quality in assessing
non-image forming effects of light.
Researchers continuously recorded pupil diameter in 16 healthy
participants (11 women), aged 16 to 30 years, with an infrared
eye-tracking device while they were given a 15-minute auditory oddball
task in a 7T fMRI scanner. Participants were concurrently exposed to
pseudo-randomly alternating 30- to 40-second blocks of polychromatic
blue (4,000 K, 200 µW/cm2) and monochromatic orange (589 nm, 6 x 1,013 photons/cm2/s) lights.
Beckers and colleagues calculated pupil response as the average pupil
size during the entire block of light, and used mixed-model analysis to
determine the effects of light condition on pupil response, with
participants as random intercept and controlling for age, sex and BMI.
Results showed that blue light was associated with a significantly smaller pupil diameter
compared with orange light (main effect of light condition: F(2,270) =
571.22). The effect of the light condition on pupil size did not
significantly change over the 15-minute protocol (light condition x
block repetition interaction: F(12,240) = 1.21), suggesting that
time-in-protocol and previous light blocks did not affect pupil
constriction.
“With light stimulation, we could modulate LC activity ... and that
will be an easy technique, easily accessible and easily handleable for
AD patients in the future,” Beckers said.
