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Infrared Light and Neurological Health
Eden Desjardins
Posted: Wednesday, September 2, 2015 11:16 AM
Joined: 5/25/2015
Posts: 48

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 : . There is more material here :

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.

Posted: Wednesday, September 2, 2015 12:55 PM
Joined: 12/20/2011
Posts: 217

Eden Desjardins wrote:

...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.

Eden Desjardins
Posted: Tuesday, September 8, 2015 8:43 AM
Joined: 5/25/2015
Posts: 48

I received the infrared transcranial device about half a week ago, I've started developing the routine of helping him put on and use the device just before his bedtime. I didn't notice any difference within the first few days.. however, to my surprise, for the past two nights, he did not wake up in the middle of the night and has told me he feels very sleepy after using the device. This is a huge relief since he had started waking up randomly over the past few months and wander around the house.

It is far too soon to tell if this was due to the device but I will keep the rest of you informed. I am keeping an eye on the calendar for my 80% refund, if this doesn't work within the six month guarantee period.

Posted: Tuesday, September 8, 2015 2:12 PM
Joined: 12/20/2011
Posts: 217

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?

Eden Desjardins
Posted: Monday, September 14, 2015 10:22 AM
Joined: 5/25/2015
Posts: 48

Definitely welcome, onward. I don't think the transcranial infrared helmet was designed to lower blood pressure but rather "photobiomodulate" neuronal mitochondria.

I'm still uncertain why this seems to be the case but from what I can tell from doing my daily research, this snippet from the research department of the US department of Veteran Affairs mentioned something about transcranial infrared light triggering better sleep in veterans with PTSD -

I think this field is personally interesting because it straddles conventional with alternative medicine.

As an update, about 1.5 weeks now and he is sleeping much better. Cognition-wise, my husband has reported saying that things seem "clearer" to him now and he is calmer. Though to me, on a scale of 1-10 I'd say the difference is about 2 to me and even still these things can be subjective. Oh well, time will tell, a little bit of improvement is better than none.

Posted: Wednesday, September 16, 2015 10:34 PM
Joined: 9/13/2013
Posts: 112

Thank you Eden for posting this.

I just spent half an hour responding to this, but upon clicking 'POST' got an error message, and lost what I wrote.

We have used a gadget using the same technolgy, but not laser. I believe your experience with this technology is not subjective. IMHO, it really works.

I will post again tomorrow to tell you of the details. It's late here 11:30 pm. .

Posted: Sunday, September 20, 2015 10:20 PM
Joined: 9/13/2013
Posts: 112

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 Reports May 2011

This 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.

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. Jan 2008.

The helmet shown here -

More 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.


Posted: Monday, September 21, 2015 6:23 AM
Joined: 7/24/2015
Posts: 3020

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.

Eden Desjardins
Posted: Monday, September 21, 2015 1:36 PM
Joined: 5/25/2015
Posts: 48

Hi scma,

Thank you for the links and pointing out the helmet designed by Dr. Dougal and Dr. Ennaceur - I had found their helmet initially based on comparing the pictures that Dr. Naeser used in Boston Medical University. I connected the dots -> improved mental cognition = offsetting Alzheimer's effects(to a certain degree).

However, I managed to find a different "next generation"transcranial infrared helmet that comes equipped with an intranasal applicator to target the underside of the brain as well. It is quite easy to put on my husband and he has been sleeping better and amazingly enough, seems less forgetful. He even remembered to take his medication for the third morning, which he wasn't able to do until recently(though he did forget yesterday).

I would say, "transcranial photobiomodulation" like you mentioned, is definitely an interesting field to delve in.. because hey, I think it's worth looking at other medicinal fields besides pharmaceuticals. Neurological pharmaceuticals are known to have a long history of negative side effects. I'm definitely not suggesting to go against prescriptions but I sometimes feel like whatever a doctor prescribes may not always be the best course of action.

The_Sun_Still_Rises, I think it's an entirely different process we're talking about. It's the use of light of precise wavelengths, pulse rate and energy levels to stimulate the mitochondria in neuronal cells back to optimal functioning level by "energizing" them.

Lane Simonian
Posted: Monday, September 21, 2015 3:59 PM
Joined: 12/12/2011
Posts: 5000

This article is on near-infrared light for Parkinson's disease but the discussion is relevant for Alzheimer's disease:

Parkinson's disease is a common progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Mitochondrial dysfunction has been strongly implicated in the pathogenesis of Parkinson’s disease. Thus, therapeutic approaches that improve mitochondrial function may prove to be beneficial. Previously, we have documented that near-infrared light via light-emitting diode (LED) treatment was therapeutic to neurons functionally inactivated by tetrodotoxin, potassium cyanide (KCN), or methanol intoxication, and LED pretreatment rescued neurons from KCN-induced apoptotic cell death...

LED treatment down-regulated nitrotyrosine expression in neurons

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.

Lane Simonian
Posted: Tuesday, September 22, 2015 10:12 AM
Joined: 12/12/2011
Posts: 5000

This one is for tinnitus but again relevant to Alzheimer's disease.

Oregon – New research reveals through a recent study a potential cure for Tinnitus Condition. The symptoms can be significantly alleviated with an noninvasive treatment calledTranscranial Magnetic Stimulation (TMS)...The results of the research were encouraging, the symptoms diminished for at least six months in half of the patients who received actual treatment instead of the placebo treatment. The research also showed that a significant part of the tinnitus patients who have had the condition for over 20 years experienced an important reduction of symptoms.

Tinnitus May Be Caused by Peroxynitrite No, Oh No!

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.”

Widespread peroxynitrite-mediated damage in Alzheimer's disease.

Posted: Tuesday, September 22, 2015 5:56 PM
Joined: 9/13/2013
Posts: 112

Eden, is your equipment made in Canada?
Here's a 2012 study that explains how low level infra red light laser works - excerpt below

"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."

Lane Simonian
Posted: Wednesday, September 23, 2015 9:49 AM
Joined: 12/12/2011
Posts: 5000

Thank you, Eden and scma for your work and shared experiences with this therapy.

Here is a critical finding:

These data indicate that 670 nm light therapy protects against nitrosative stress and apoptosis within the central nervous system, contributing to the clinical effect of 670 nm light therapy previously noted in the EAE [experimental autoimmune encephalomyletis] model.

Some of the consequences of nitrostatvie stress in Alzheimer's disease are reduced blood flow, decreased synaptic plasticity, and inhibited neurogenesis due to the nitration of the catalytic subunit of the the neuroprotective phosphatidylinositol 3-kinase and interference with neurotransmissions and the transport of nutrients in the brain due to the nitration of tau proteins. Anything which slows down nitration will slow down the progression of Alzheimer's disease. Strong peroxynitrite scavengers such as panax ginseng and aromatherapy with essential oils high in eugenol will partially reverse nitration and should partially reverse Alzheimer's disease.

Eden Desjardins
Posted: Monday, September 28, 2015 11:52 AM
Joined: 5/25/2015
Posts: 48

Yes, scma. The equipment I use on my husband is made by a Canadian company.

Lane, thank you for that find, that was an excellent read. There seems to be a lot of research in regards to nerve and neurons(which happen to be nerves) responding positively to near infrared light.


Here is an article by the the University of Texas at Austin Institute for Neuroscience - Link to Article

"Barrett & Gonzalez-Lima (2013) discovered that transcranial laser stimulation can enhance sustained attention and short-term memory in humans. We extend this line of work to executive function. Specifically, we ask whether transcranial laser stimulation enhances performance in the Wisconsin Card Sorting Task (WCST) that is considered the gold-standard of executive function and is compromised in normal aging and a number of neuropsychological disorders. We used a laser of a specific wavelength (1064 nm) that photostimulates cytochrome oxidase—the enzyme catalyzing oxygen consumption for metabolic energy production. Increased cytochrome oxidase activity is considered the primary mechanism of action of this intervention. Participants who received laser treatment made fewer errors and showed improved set-shifting ability relative to placebo controls. These results suggest that transcranial laser stimulation improves executive function and may have exciting potential for treating or preventing deficits resulting from neuropsychological disorders or normal aging."

Here is another brilliant article I could find too :

Photobiomodulation directly benefits primary neurons functionally inactivated by toxins: role of cytochrome c oxidase.

"Far red and near infrared (NIR) light promotes wound healing, but the mechanism is poorly understood. Our previous studies using 670 nm light-emitting diode (LED) arrays suggest that cytochrome c oxidase, a photoacceptor in the NIR range, plays an important role in therapeutic photobiomodulation. If this is true, then an irreversible inhibitor of cytochrome c oxidase, potassium cyanide (KCN), should compete with LED and reduce its beneficial effects. This hypothesis was tested on primary cultured neurons. LED treatment partially restored enzyme activity blocked by 10-100 microm KCN. It significantly reduced neuronal cell death induced by 300 microm KCN from 83.6 to 43.5%. However, at 1-100 mm KCN, the protective effects of LED decreased, and neuronal deaths increased. LED significantly restored neuronal ATP content only at 10 microm KCN but not at higher concentrations of KCN tested. Pretreatment with LED enhanced efficacy of LED during exposure to 10 or 100 microm KCN but did not restore enzyme activity to control levels. In contrast, LED was able to completely reverse the detrimental effect of tetrodotoxin, which only indirectly down-regulated enzyme levels. Among the wavelengths tested (670, 728, 770, 830, and 880 nm), the most effective ones (830 nm, 670 nm) paralleled the NIR absorption spectrum of oxidized cytochrome c oxidase, whereas the least effective wavelength, 728 nm, did not. The results are consistent with our hypothesis that the mechanism of photobiomodulation involves the up-regulation of cytochrome c oxidase, leading to increased energy metabolism in neurons functionally inactivated by toxins."

In relation to Alzheimer's, I believe we can equate the re-activation of neurons functionally inactivated by toxins to the inactivated/damaged neurons commonly found in Alzheimer's patients. So, this may offset the negative memory-reducing effects of Alzheimer's.


My own personal theory is somewhere along the course of evolution, mitochondria(the "batteries" of our cells) have evolved to utilize infrared light from the sun (radiation from the sun or sunlight, is a mixture of electromagnetic waves ranging from infrared to ultraviolet rays).

What I love about this therapy is that it seems to offer so much promise, without the usual side effects that come from pharmaceuticals(nausea, vomiting, diarrhea, fatigue, weight loss, muscle cramps... etc). Hopefully, more research gets done

Eden Desjardins
Posted: Monday, December 14, 2015 11:29 AM
Joined: 5/25/2015
Posts: 48

Hello everyone,


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 :


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.

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

Lane Simonian
Posted: Monday, December 14, 2015 8:09 PM
Joined: 12/12/2011
Posts: 5000

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.

Low-Level Laser Therapy (808 nm) Reduces Inflammatory Response and Oxidative Stress in Rat Tibialis Anterior Muscle After Cryolesion




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).

Posted: Sunday, December 20, 2015 1:41 PM
Joined: 9/13/2013
Posts: 112

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.




Eden Desjardins
Posted: Monday, December 21, 2015 11:46 AM
Joined: 5/25/2015
Posts: 48

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.

Lane Simonian
Posted: Tuesday, December 22, 2015 1:02 PM
Joined: 12/12/2011
Posts: 5000

Here is one more important piece of the puzzle:

Persistent Mitochondrial Damage by Nitric Oxide and its Derivatives: Neuropathological Implications

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.

Eden Desjardins
Posted: Monday, January 4, 2016 11:43 AM
Joined: 5/25/2015
Posts: 48

Hi Lane,

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 :


This article explains the link between photobiomodulation, cytochrome c oxidase and nitrite levels. 

"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. 

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, unpublished results)"

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.

Posted: Wednesday, January 13, 2016 8:08 PM
Joined: 1/24/2015
Posts: 6

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??? 

Lehman Hoag

Mimi S.
Posted: Thursday, January 14, 2016 8:49 AM
Joined: 11/29/2011
Posts: 7027

A certain percentage of folks with MCI never progress to full blown dementia. Hopefully you are in that group.

Posted: Friday, January 15, 2016 5:55 AM
Joined: 4/24/2012
Posts: 484

Ihoagjr, I have seen several studies supporting the benefits of Melatonin for Alzheimer's. I will look for them and post in a separate topic. As I recall it works on the level of amyloid in the cell (removal or prevention, or antioxidant) and maybe a connection to getting good sleep as well. Don't know if there are any down sides to taking it.
Posted: Monday, March 6, 2017 3:03 PM
Joined: 3/6/2017
Posts: 1

Thank you for sharing your husband's progress on Photobiomodulation.  our brother has frontotemporal dementia (FTD) and was given 3-5 years to live.  I did see an article by Dr Mercola on Photobiomodulation.  would you mind giving an update on your husband's progress using the Photobiomodulation equipment?  where did you purchase it?  i've also read and infrared sauna's help as well since it will release toxins...has your husband ever tried that?


thank you so very much!
Posted: Tuesday, December 5, 2017 10:54 AM
Joined: 12/5/2017
Posts: 1

In retrospect, do you think the helmet is something you would recommend?

where would I look for it?

 Thank you. 

Posted: Monday, January 1, 2018 5:04 PM
Joined: 1/1/2018
Posts: 209

I just ordered a VieLight intranasal device for my mother.  There was an artical about this device in AARP circular.  I am desperate right now.  Mom gets agitated and disoriented about 3:00 every afternoon.  I close the drapes but it doesn't seem to help.  The device was $500 but I received a 10% discount with an "AARP" discount code.  Of course after I ordered it I found out that one of the doctors that is working with these devices is a quack and benefits from the sale of these devices.  But at this point I think $500 is a small price to pay if there is any improvement.
Posted: Monday, January 1, 2018 5:13 PM
Joined: 1/1/2018
Posts: 209

Hello, I just ordered the nasal equipment from VieLight.  What they wanted me to do was order the model that cradles the head, probably something like a helment.  It was $1750 though so I decided to order the cheaper nasal model.  VieLight is a Canadian company.  They promise an 80% refund in 6 mos if you are not satisfied.