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Infrared Light and Neurological Health
Transcranial absorption of photon energy by cytochrome oxidase, the terminal enzyme in mitochondrial respiration, is proposed as the bioenergetic mechanism of action of photobiomodulation in the brain. Transcranial photobiomodulation up-regulates cortical cytochrome oxidase and enhances oxidative phosphorylation.
Photobiomodulation improves prefrontal cortex-related cognitive functions, such as sustained attention, extinction memory, working memory, and affective state. Transcranial infrared stimulation may be used efficaciously to support neuronal mitochondrial respiration as a new non-invasive, cognition-improving intervention in animals and humans. This fascinating new approach should also be able to influence other brain functions depending on the neuroanatomical site stimulated and the stimulation parameters used.
Healthy volunteers received continuous wave near-infrared light intersecting cytochrome oxidase's absorption spectrum, delivered to the forehead using a 1064 nm low-power laser diode (also known as “cold laser”), which maximizes tissue penetration due to its long wavelength, and has been used in humans for other indications. The power density (or irradiance), 250 mW/cm2, as well as the cumulative energy density (or fluence), 60 J/cm2, were the same that showed beneficial psychological effects in Schiffer et al..
This laser exposure produces negligible heat and no physical damage at the low power level used. This laser apparatus is used safely in a clinical setting by the supplier of the laser (Cell Gen Therapeutics, HD Laser Center, Dallas, TX). Reaction time in the PVT was improved by the laser treatment, as shown by a significant pre-post reaction time change relative to the placebo group.
The DMS memory task also revealed significant enhancements in measures of memory retrieval latency and number of correct trials, when comparing the infrared-treated with the placebo group (Figure (Figure1).1). Self-reported positive and negative affective (emotional) states were also measured using the PANAS-X questionnaire before and 2 weeks after laser treatment. As compared to the placebo, treated subjects reported significantly improved affective states. We suggest that this kind of transcranial laser stimulation may serve as a non-invasive and efficacious method to augment cognitive brain functions related to attention, memory, and emotional functions.
I have summarized material I found from this article here : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953713/ . There is more material here : https://en.wikipedia.org/wiki/Transcranial_photobiomodulation
I believe they may be on to something via utilizing infrared light to stimulate neuronal health. I am going to give transcranial infrared photobiomodulation a try for my husband, since he is still in the early stages of Alzheimer's.
...I believe they may be on to something via utilizing infrared light to stimulate neuronal health. I am going to give transcranial infrared photobiomodulation a try for my husband, since he is still in the early stages of Alzheimer's.
Eden, thanks for posting about this new approach and please let us know how things work out. Wishing you & your husband all the best.
Thanks very much for the update. It'll be interesting to see how things go from here.
You said he feels very sleepy after using it. I wonder if it lowers blood pressure. (Could be a concern in some people, but a help to others.)
And how much does the device cost?
The infra red light was also used to treat Traumatic Brain Injury. The study -Improved Cognitive Function After Transcranial, Light-Emitting Diode Treatments in Chronic, Traumatic Brain Injury: Two Case Reportshttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104287/ May 2011This study was #21 in the Reference section of your posted wiki article. The article refer to it stating two patients with TBI were treated using infra red light. https://en.wikipedia.org/wiki/Transcranial_photobiomodulation. I contacted Dr Naeser (Ph D) and Ms Saltmarche (RN) in September 2012 and was able to get the medical equipment used. I chose the equipment because of the way it was used - the equipment is applied in several acupuncture points which has a synergy effect. We had my nephew use the equipment on my mom who has moderate alzheimer once a week when he is available. One obvious effect is that she is calmer and sleep better when she gets the treatment. But we have not consistently used the treatment as we rely on my nephew's schedule. Your post is a reminder for us to use it regularly on a frequent basis. The first idea of using low level infra red light (1072 nm) for alzheimer was first initiated by Dr Dougal & Dr Ennaceur at University of Sunderland in Northeast England. http://www.sunderland.ac.uk/newsevents/news/news/index.php?nid=468 Jan 2008. The helmet shown here - http://www.dailymail.co.uk/health/article-510172/The-helmet-turn-symptoms-Alzheimers.htmlMore recent researches confirm that the use of low level infra red light help Alzheimer's especially in the early stage. And it's getting a fancy name - Transcranial photobiomodulation.
It might have something to do with the fact that the blue light from phones, computers, and TV is disrupting to our day/night rhythm.
Interesting the results you guys are getting.
I make sure to use light bulbs that emit yellow (as opposed to blue) light...usually slightly more expensive bulbs if using LED. I notice a big difference in calm at home for all of us.
Nitrotyrosine is an indicator of cell damage and results from the nitration of tyrosine residues in proteins by peroxynitrite, a product of nitric oxide and superoxide. The expression of nitrotyrosine was at a low level (10.5%) in normal primary cultures. However, the number of nitrotyrosine-positive neurons increased significantly after exposure to 300 µM of KCN for 3 days (P P Fig. 4F)...
In summary, our results demonstrate that LED treatment twice a day was more effective in increasing the cellular ATP content and cytochrome oxidase activity and rescuing neurons from toxin-induced cell death. Twice a day LED treatment significantly counteracted both rotenone-and MPP+-induced neurotoxicity. Optimizing endogenous energy production and protecting neurons from neurotoxin-induced cell death are worthy measures to be considered in PD treatment and clinical therapy.
A very recent paper1 proposes that tinnitus, as well as diseases such as chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, and posttraumatic stress disorder, may be caused by a “vicious-cycle mechanism known as the NO/ONOO– (‘no, oh no!’) cycle mechanism.”1 ONOO– (peroxynitrite) is the “oh no!” part of the cycle and is created by the chemical reaction between superoxide radicals and nitric oxide (NO). The authors note that “Tinnitus is also comorbid [i.e., occurs at the same time] with these illnesses, and these are comorbid with one another, suggesting a possible common etiology.”
"The current hypothesis for NILT's efficacy is based upon a two-step process: the light first elicits an acute response, followed by a chronic response in which activation of neuronal survival and plasticity mechanisms achieves a long-term effect. These responses are not related to heating of tissue, which is minimal, but appear to be wavelength-specific, being effective when NILT is used at wavelengths of 630nm or 808nm. Both of these wavelengths correspond to absorption peaks of a vital mitochondrial enzyme called cytochrome c oxidase (COX).
The acute phase response by photobiostimulation directly affects cellular metabolic activity regulated within mitochondria. Specifically, NILT increases adenosine triphosphate (ATP) formation in brain cells after COX (and perhaps other enzymes) absorb photons of the light. ATP is the unit of fuel that delivers the energy needed by innumerable cellular processes. Usually mitochondria produce ATP efficiently by aerobic respiration. In AIS or TBI, neuronal tissue deprived of oxygen may survive for some time by switching to less-efficient anaerobic respiration. We hypothesize that the mitochondrial stimulation by NILT may help cells to switch back to aerobic respiration, improving the cell's chances for recovery. In AIS, NILT may also increase cerebral blood flow, which ultimately allows cells to receive more oxygen and nutrients.
The chronic response of NILT appears to have long-term effects by also increasing RNA transcription and protein synthesis, activating mechanisms that aid in alleviating injury-induced brain dysfunction. NILT may have a direct or indirect effect on synaptic plasticity and possibly neurogenesis. In addition, NILT-induced suppression of inflammatory responses may be partly responsible for chronic effects of the treatment. Animal studies have shown NILT to be neuroprotective and able to restore function following various brain insults and in various diseases, such as TBI, Alzheimer's, and Parkinson's. Common mechanisms may underlie NILT's beneficial effects on neuronal survival and enhanced clinical function in these disparate pathologies."
Yes, scma. The equipment I use on my husband is made by a Canadian company.
It's been awhile since I've written here. I have been tracking research updates on photoneuromodulation quite obsessively because of the potential I believe it holds for dementia related diseases and I have noticed improvements in my husband's memory and especially his behaviour, albeit minimal - it's definitely doing something.
I was lucky enough to stumble across a very compelling educational youtube video about the science of "photoneuromodulation" or "photobiomodulation" and its' beneficial effects on the human brain. Link for those interested : https://www.youtube.com/watch?v=46oBjzW5OJM
Here is an in depth paper about the mathematical side of photobiomodulation and transcranial NIR penetration, published on the 19th of March 2015. According to this paper, the nasal cavity is the most efficient method for reaching the deeper brain structures.https://www.researchgate.net/publication/273781132_Red_and_NIR_light_dosimetry_in_the_human_deep_brain
Federal Institute of Technology (EPFL), Institute of Chemical Sciences
and Engineering (ISIC), 1015 Lausanne, Switzerland
2 Medos International Sàrl, Chemin Blanc 38, 2400 Le Locle, Switzerland
Photobiomodulation (PBM) appears promising to treat the hallmarks of
Parkinson’s Disease (PD) in cellular or animal models. We measured light
propagation in different areas of PD-relevant deep brain tissue during
transcranial, transsphenoidal illumination (at 671 and 808 nm) of a cadaver
head and modeled optical parameters of human brain tissue using MonteCarlo
simulations. Gray matter, white matter, cerebrospinal fluid, ventricles,
thalamus, pons, cerebellum and skull bone were processed into a mesh of the
skull (158 × 201 × 211 voxels; voxel side length: 1 mm). Optical parameters
were optimized from simulated and measured fluence rate distributions. The
estimated μeff for the different tissues was in all cases larger at 671 than at
808 nm, making latter a better choice for light delivery in the deep brain.
Absolute values were comparable to those found in the literature or slightly
smaller. The effective attenuation in the ventricles was considerably larger than
literature values. Optimization yields a new set of optical parameters better
reproducing the experimental data. A combination of PBM via the sphenoid
sinus and oral cavity could be beneficial. A 20-fold higher efficiency of light
delivery to the deep brain was achieved with ventricular instead of transcranial
illumination. Our study demonstrates that it is possible to illuminate deep
brain tissues transcranially, transsphenoidally and via different application
routes. This opens therapeutic options for sufferers of PD or other cerebral
diseases necessitating light therapy.
The objective of the present study was to refine a possible treatment option for PD patients,
in a human cadaver model. We wanted to validate the practicalities of light delivery by illuminating
the SNpc transcranially and transsphenoidally. We also wanted to validate the light
dosimetry by quantifying light distribution within the target brain tissue when illumination
takes place from the nasal cavity under endoscopic guidance. To this end, we measured fluence
rate distribution in selected intracranial locations while delivering light at two different
wavelengths from a location outside the skull and accessible by an endoscope. Our study
demonstrates that this approach is possible.
We showed experimentally that the transsphenoidal delivery of light to the relevant target
structures of the brain is possible. Our measurements allowed us to validate the model by
directly measuring the fluence rate within the target brain structures and to experimentally
determine the optical parameters of the brain tissues in this specimen. These will add to an
existing body of data and we hope they will be useful to refine published parameters that are
notoriously subject to large variations due to experimental conditions or to the specifics of a
given specimen. Finally, our study allowed us to determine the light dose delivered to the deep
brain for different application routes, a result that could open a number of therapeutic options
for PD patients as well as for sufferers of other cerebral disease necessitating light therapy
delivered in a non-invasive way
Thank you for updating us, Eden. I think one of the greatest myths of Alzheimer's disease is that nothing can be done to treat it. Any improvement is important.
I am listening to the video as I type. I found this bit of information which may partially explain the value of photobiomodulation.
LLLT reduced oxidative and nitrative stress in injured muscle, decreased lipid peroxidation, nitrotyrosine formation and NO production, probably due to reduction in iNOS protein expression. Moreover, LLLT increased SOD gene expression, and decreased the inflammatory response as measured by gene expression of NF-kβ and COX-2 and by TNF-α and IL-1β concentration.
These results suggest that LLLT could be an effective therapeutic approach to modulate oxidative and nitrative stress and to reduce inflammation in injured muscle.
Oxidative and nitrative stress are critical contributors to Alzheimer's disease. They reduce blood flow and the transport of glucose in the brain, inhibit the synthesis and release of neurotransmitters governing short-term memory, sleep, mood, social recognition, and alertness, inhibit the regeneration of neurons in the hippocampus, and contribute to mitochondrial dysfunction (I am pleased to see that the video touches upon some of this).
T Thanks Eden for the video link. And the 'nasal' study.
It seems that the nasal cavity is the best way to reach the brain, this is how aromatheraphy works. Knowing infra red light can also use the same path is a great discovery. Hopefully more randomized clinical trials are done to show its effectiveness in the human brain.
Lane, I do agree that prolonged oxidative and nitrative stress definitely has a negative effect on the brain - leading to sustained inflammation, cellular proliferation and cytotoxicity in brain cells. If "photobiomodulation" can relieve these factors even by a minimal amount, worth a shot.
There is a direct correlation between the animal cells in used the study you refer to.. which I believe is the existence of mitochondria within both muscle and neuronal cells.From - Link"Evidence that mitochondrial cytochrome c oxidase is the primary photoreceptor for photobiomodulation initially came from the finding that most of the light absorbed by cells is absorbed by mitochondrial cytochrome c oxidase (and, to a lesser extent, by other mitochondrial pigments) (Beauvoit et al., 1994), and from a determination of the action spectrum on NIR light on cell proliferation and cell attachment (Karu, 1999; Karu et al., 2005). Additional evidence for the involvement of mitochondrial cytochrome c oxidase in photobiomodulation has come from several studies with neuronal cells and tissues. These studies have demonstrated: (1) that light at 670 nm reverses the ability of tetrototoxin, a sodium channel blocker, to diminish mitochondrial cytochrome c oxidase activity in neuronal cells (Wong-Riley et al., 2001); and (2) that NIR light reverses the toxic effects of methanol on mitochondrial cytochrome c oxidase in rat retinas, resulting in improved vision (Eells et al., 2003). More direct evidence for the involvement of cytochrome c oxidase in photobiomodulation comes from studies on neuronal celldeath (Wong-Riley et al., 2005). These studies examined whether inhibitors of mitochondrial cytochrome c oxidase could compete with NIR treatment. The results from these studies indicated that NIR light could protect neuronal cells from induced cell death by potassium cyanide, a potent cytochrome c oxidase inhibitor. These studies, done under normoxic conditions, also revealed that the most effective wavelengths paralleled the NIR absorption spectrum of oxidized cytochrome c oxidase. When considered together, these studies provide compelling evidence that mitochondrial cytochrome c oxidase is a primary photoreceptor for photobiomodulation."
The question I'm pondering about is whether photobiomodulation is merely mitigating the effects of Alzheimer's disease or actually addressing the issue. I guess we won't ever know, since scientists still don't actually know what causes Alzheimer's.
scma : Yes, the underside of the brain contains the structures related to long term-memory, so the intranasal piece is the most important, in my opinion.
Here is one more important piece of the puzzle:
Approximately 15 years ago we reported that cytochrome c oxidase (CcO) was persistently inhibited as a consequence of endogenous induction and activation of nitric oxide (•NO) synthase-2 (NOS2) in astrocytes. Furthermore, the reactive nitrogen species implicated was peroxynitrite. In contrast to the reversible inhibition by •NO, which occurs rapidly, in competition with O2, and has signaling regulatory implications, the irreversible CcO damage by peroxynitrite is progressive in nature and follows and/or is accompanied by damage to other key mitochondrial bioenergetic targets. In purified CcO it has been reported that the irreversible inhibition occurs through a mechanism involving damage of the heme a3-CuB binuclear center leading to an increase in the Km for oxygen. Astrocyte survival, as a consequence of peroxynitrite exposure, is preserved due to their robust bioenergetic and antioxidant defense mechanisms. However, by releasing peroxynitrite to the neighboring neurons, whose antioxidant defense can, under certain conditions, be fragile, activated astrocytes trigger bioenergetic stress leading to neuronal cell death. Thus, such irreversible inhibition of CcO by peroxynitrite may be a plausible mechanism for the neuronal death associated with neurodegenerative diseases, in which the activation of astrocytes plays a crucial role.
The critical question is how well does biophotomodulation inhibit this process.
That article is interesting and points to the link between mitochondria/cytochrome c oxidase and neuronal death through irreversible preoxynitrite inhibition.
"However, by releasing peroxynitrite to the neighboring neurons, whose antioxidant defense can, under certain conditions, be fragile, activated astrocytes trigger bioenergetic stress leading to neuronal cell death. Thus, such irreversible inhibition of CcO by peroxynitrite may be a plausible mechanism for the neuronal death associated with neurodegenerative diseases, in which the activation of astrocytes plays a crucial role. "
You may find this article interesting : https://www.researchgate.net/publication/50225298_Therapeutic_photobiomodulation_Nitric_oxide_and_a_novel_function_of_mitochondrial_cytochrome_c_oxidase
This article explains the link between photobiomodulation, cytochrome c oxidase and nitrite levels.
examined whether inhibitors of mitochondrial
cytochrome c oxidase could compete with NIR treatment.
The results from these studies indicated that NIR
light could protect neuronal cells from induced cell
death by potassium cyanide, a potent cytochrome c oxidase
Several studies have implicated nitric oxide in photobiomodulation.
These range from the finding that
human monocytes release nitric oxide when exposed to
NIR light (Lindgard et al., 200 to the finding that different
wavelengths of NIR light have differential effects
on the expression of inducible nitric oxide synthase
(Moriyama et al., 2005; 2009). In a recent study, it has
been reported that NIR could protect cardiomyocytes
from hypoxia and reoxygenation damage, and that this
protection involves nitric oxide (Zhang et al., 2009).
This study also reported that not all of the nitric oxide
involved is produced by nitric oxide synthases. The
finding that some of the nitric oxide is not produced by
nitric oxide synthases is interesting because of the
recently discovered Cco/NO activity of cytochrome c
oxidase. Indeed, this activity provides an alternative
enzymatic source of cellular nitric oxide.
Early studies revealed that Cco/NO activity is inhibited
by high oxygen concentrations and functions primarily
under hypoxic conditions (Castello et al., 2006).
However, more recent studies have revealed that
Cco/NO activity can be modulated and functions over a
wide range of oxygen concentrations. For example,
studies with yeast have demonstrated that Cco/NO
activity is differentially affected by the oxygen-regulated
isoforms of cytochrome c oxidase (Castello et al.,
200. Cytochrome c oxidase carrying the aerobic isoform,
Va, of yeast subunit V (mammalian subunit IV-1)
has Cco/NO activity which is optimal at oxygen
concentrations below 20 μM O2, an oxygen level that is
within the hypoxic range for most tissues (van Faassen
et al., 2009). In contrast, cytochrome c oxidase carrying
the hypoxic oxygen regulated-subunit isoform, Vb, of
yeast subunit V (mammalian subunit IV-2) has Cco/NO
activity that functions at oxygen concentrations as high
as 160 μM O2 (Castello et al., 200, which is well
within the normoxic range for many mammalian tissues
(van Faassen et al., 2009). An elevated ratio of
ADP/ATP also alters the oxygen sensitivity of Cco/NO
in both yeast and mammalian mitochondria, allowing
an enzyme with the aerobic oxygen-regulated
cytochrome c oxidase subunit isoform to produce nitric
oxide under normoxic conditions (Castello and Ball,
Not completely related to the inhibition of preoxynitrite but the neuroprotective effects against potassium cyanide(another potent cytochrome c oxidase inhibitor) certainly seems promising.
What is most striking about transcranial-intranasal photobiomodulation (or photoneuromodulation) is the lack of side effects that usually accompanies drugs as well. There aren't any downsides to giving it a try.
I use the cheep sleep aid Melatonin to avoid the progression of Alz. I was classed MCI over a year ago and still am not progressing into stage one!! There was a study in 1990 done on the use of Melatonin, but since it has been classified as a sleep aid, no notice of it being used to STOP THE PROGRESSION OF ALZ. I still can drive, do the dishes, clean our condo, etc. Why haven't I progressed? Why???
In retrospect, do you think the helmet is something you would recommend?
where would I look for it?