Science by press release: A helmet to fight Alzheimer’s disease?


Recently, I’ve had a number of people bring to my attention a news story that has apparently been sweeping the wire services and showing up in all sorts of venues. It is, on its surface, a story of hope, hope for the millions of elderly (and even the not-so-elderly) who are or will be afflicted by that scourge of the mind, memory, and personality, Alzheimer’s disease. This disease is one of the most feared of diseases. A progressive and fatal disease of the brain, it robs a person of his memory and personality, until he no longer recognizes loved ones and becomes too demented to care for himself. The pathophysiology involves the accumulation in the brain of a protein known as β-amyloid, which forms plaques outside of cells, while neurofibrillary tangles believed to be due to the hyperphosphorylation of a protein known as tau develop in dying cells. The exact mechanism by which neuron death occurs is not fully understood, but over time this process leads to a decrease in the amount of gray matter in the cortex. There is no known cure, and the current treatments that we have result in at best a modest delay of the inevitable dementia that accompanies progression of the disease.

Given this grim backdrop and the general aging of the population in developed nations, it is expected that there will be a large increase in the number of people developing Alzheimer’s disease over the next few decades. Naturally, this provides a great deal of incentive to develop more effective treatments. Not surprisingly, sometimes the treatments proposed may sound somewhat outlandish and may even be somewhat outlandish. The treatment about which people were e-mailing me falls into this category, and I haven’t decided yet whether it’s science or pseudoscience. It could be legitimate. What I do know, however, is that I don’t like the way its inventors are promoting it by press conference before any evidence of its clinical efficacy in humans has been accepted by a peer-reviewed publication, leading to a flurry of stories about a new possible “miracle cure” for Alzheimer’s disease grounded in not a lot of science. I’m referring, of course, to the “Alzheimer’s helmet” developed by Dr. Gordon Dougal and his colleagues Dr. Paul Chazot and Abdel Ennaceur at Durham University. Dr. Dougal is a director of Virulite, a medical company based in County Durham in the U.K. Here’s a widely cited article from the Daily Mail that describes the device:

An experimental helmet which scientists say could reverse the symptoms of Alzheimer’s disease within weeks of being used is to be tried out on patients.

The strange-looking headgear – which has to be worn for ten minutes every day – bathes the brain with infra-red light and stimulates the growth of brain cells.

Its creators believe it could reverse the symptoms of dementia – such as memory loss and anxiety – after only four weeks.

Alzheimer’s disease charities last night described the treatment as “potentially life- changing” – but stressed that the research was still at the very early stages.

My first thought upon reading this it sounds too good to be true. The brain damage due to Alzheimer’s disease takes years, if not decades, to develop to the point where the patient starts to show syptoms of cognitive decline. To think that it would be reversed within weeks borders on magical thinking. My second thought was that they’re just heating up the brain with infrared radiation. I have to admit that my second thought was wrong, mainly because I somehow neglected to notice the “near” in front of the “infrared.” This makes a difference. Far infrared (IR-C) is light with a wavelength from 3000 nm to 1.0 mm and is used in thermal imaging. It’s mainly detected by humans as heat. However, near infrared (NIR) is much closer to the wavelengths that the human eye can see and encompasses a range from 700 to 1400 nm. This is the wavelength range that is commonly used in night vision goggles and, increasingly, in medical imaging. Indeed, one area of active research is to use near infrared spectroscopy (NIRS) to differentiate benign from cancerous breast lesions; the cancerous lesions tend to be warmer due to increased blood flow due to increased angiogenesis. It can also be used to measure oxygen content in the blood and even cerebral bloodflow, although the interference of the skull and other bones remains a significant problem, limiting the accuracy greatly for depths of more than 3 cm or so. However, this technique has nonetheless been successfully  used in Alzheimer’s disease patients to measure differences in cerebral blood flow.

All of this is well and good, but it does not necessarily mean that near infrared radiation delivered through a helmet that looks like something out of Tron is going to reverse the changes in Alzheimer’s disease. On what do these scientists base their bold claim? Let’s see:

Dr. Dougal claims that only ten minutes under the hat a day is enough to have an effect.

“Currently all you can do with dementia is to slow down the rate of decay – this new process will not only stop that rate of decay but partially reverse it,” he said.

Low level infra-red red is thought to stimulate the growth of cells of all types of tissue and encourage their repair. It is able to penetrate the skin and even get through the skull.

“The implications of this research at Sunderland are enormous – so much so that in the future we could be able to affect and change the rate at which our bodies age,” he said.

“We age because our cells lose the desire to regenerate and repair themselves. This ultimately results in cell death and decline of the organ functions – for the brain resulting in memory decay and deterioration in general intellectual performance.

“But what if there was a technology that told the cells to repair themselves and that technology was something as simple as a specific wavelength of light?”

I did so want to believe this research, but Dr. Dougal has just told us that it’s based on a single mouse study and extrapolation from research in other systems that shows that NIR can be useful for accelerating the healing of chronic wounds. There’s just one problem. Wound healing involves the proliferation of many cell types and the ingrowth of new blood vessels. Neurons are terminally differentiated. Although there is some plasticity and there may be some small ability to regenerate, in the elderly once a neuron is dead, it’s dead, and it won’t be replaced. Unless the lost neurons in Alzheimer’s disease patients can be replaced, it’s hard to imagine how NIR could truly reverse the dementia due to it, no matter what its effects on the remaining living neurons might be. True, it’s possible, based on work showing that NIR can have therapeutic effects on neurons in tissue culture poisoned by cyanide or tetrodotoxin and can increase ATP formation in rat brains, to see how this therapy might–I repeat, might–slow or temporarily improve the course of cognitive decline. However, that’s about it as much as can be imagined for this therapy, even if all the claims for it are true, given the available evidence.

AFter seeing Dr. Dougal’s claims, I couldn’t resist looking up the actual research paper upon which they based them and to dig deeper. The study to which the Daily Mail article refers was recently published in Neurobiology of Learning and Memory1. In the study, Michalikova et al used a special strain of mouse known as CD1. This strain of mouse was chosen because it shows a high frequency of systemic amyloidosis. I’m not an expert on Alzheimer’s research, but CD1 doesn’t appear to be one of the mouse models for Alzheimer’s disease listed on the Jackson Laboratory website. Be that as it may, these mice apparently show a high incidence of age-related cognitive difficulties in common maze tests, leading the authors to propose them as a “model for age-related disorders,” despite the fact that it has not been shown that the amyloid deposits in the brains of these mice.

The experimental design was fairly simple. Middle-aged mice were placed in special boxes that administered whole body treatment of NIR at 1,072 nm for six minutes, while control mice were placed in the box for the same amount of time without the NIR. The third group included young mice who were not exposed to NIR as a baseline, to see if NIR could align the performance of the middle-aged mice to that of the young mice. The mice were then introduced to a rather imposing-looking 3D maze with eight different arms without prior habituation. Repeated sessions were done to test the effects of habituation on performance. NIR had no effect on exploratory activity or anxiety responses, but did appear to improve tasks related to memory acquisition in the maze to almost as good as the young CD1 mice. Not being a neuroscientist or psychologist, I can’t comment on the validity of this particular maze model. One oddity that I noted was that the NIR-treated middle-aged mice seemed to do the task more slowly, although their memory of the maze appeared improved. In other words, the navigated the maze more slowly, but more accurately. The authors attributed this to the mice being more “considerate” in their decision-making of what arm to enter.

This is pretty much all the major evidence upon which Dr. McDougal bases his claim for his LED-filled helmet. Well, not quite. He does claim to have some human data:

“It was becoming obvious to us that this wavelength of light was capable of various therapeutic effects, the most unusual of which was to enhance cerebral activity. Gordon observed that after irradiating his brain (5% of the light is transmitted through the skull) his mental agility was improved,” he commented.

With ethics committee approval, they commenced treatment of patients with dementia and although they recruited only a small cohort, they were able to observe an improved standard mini-mental score after six weeks of treatment lasting 20 minutes every second or third day. At the same time the volunteer’s carers observed an improvement with patients becoming more spontaneously sociable as treatment progressed.

I understand that this was a pilot study. What I don’t understand is why Dr. Dougal went to the press with it, instead of submitting it for publication in a peer-reviewed journal. On second thought, I can guess why. This does not appear to have been a randomized, double-blinded trial, but simply a tiny trial of six patients. As for the apparent improvements in sociability observed in the test subjects amd himself when self-experimenting, a better example of probable confirmation bias I would be hard-pressed to find. Given the highly preliminary data and the unclear control for counfounding factors leading to the apparent improvement, such as the added attention of undergoing treatment over other day or mild improvement with repetition of the cognitive, it’s unlikely a good journal would have published it. This is the sort of intervention that would in principle be pretty straightforward to test in a randomized, double-blind, controlled clinical trial. All that would have to be done is to design a helmet apparatus where a technician could turn program it either to actually administer the NIR or not and then leave unseen before the technician and the patient come into the room. Then, neither the techician, the patient, nor the patient’s caregiver would know whether the patient received the “real” NIR or the sham NIR. That’s what it would take to give a clear demonstration that this device can do what is claimed for it.

This story illustrates why science by press release is a huge red flag when it comes to assessing the reliability of a scientific study–any scientific study. It’s imperative whenever you see such a story to ask at least three questions:

  • Has the the study actually been published in a peer-reviewed journal? Or, at the very least, has it been presented at a reputable scientific meeting, preferably as a talk (for which the peer-review is more rigorous) rather than a poster (which is usually pretty easy to get accepted)? If the study has not been presented in a journal or scientific meeting, then it’s not unreasonable to wonder why.
  • Is there a potential conflict of interest or financial consideration? In this case there is. Dr. Dougal is the director of Virulite, a product that uses NIR to treat cold sores, which are caused by a herpes virus. It’s very clear that, in the case of the Virulite Alzheimer’s helmet, his company is trying to develop a product to market.
  • If the answer to any or all of the above questions is “yes,” ask: Why is this press release being made now? In the case of this helmet, I can only speculate, but the answer that immediately comes to mind is that Virulite is looking for investors to fund the development of the helmet. That is by far the most likely reason why this embryonic product is being publicized now.

Yes answers to any or all of the above questions do not necessarily mean that the helmet is pseudoscientific. Clearly, it’s not. After all, there’s a potential mechanism and there is animal data to suggest that it might have beneficial effects on cognitive function. (Without publication of detailed methods and results for the small trial in humans, I will not consider that data in evaluating this device, nor should you.) However, it is very much unproven, and Dr. Dougal is engaging in a great deal of hyperbole about NIR as a therapeutic modality for Alzheimer’s disease (“this new process will not only stop that rate of decay but partially reverse it”). His associate James Haslam has even claimed that NIR could be an antiaging treatment and “enhance local or systemic immunity” or even treat viral meningitis or encephalitis, all of which are claims for which there is no direct evidence–even if the mouse study is completely correct. Sadly, the hype surrounding this device is far more salesmanship than science, and patients with Alzheimer’s disease and their families deserve better. It’s a shame that Dr. Dougal and his co-investigators chose to take the route of science by press release to raise money for what is an interesting and potentially promising albeit risky line of research.


1. Michalikova S, Ennaceur A, van Rensburg R, Chazot PL (2007). Emotional responses and memory performance of middle-aged CD1 mice in a 3D maze: Effects of low infrared light. Neurobiol. Learning Mem. E-pub ahead of print.

Posted in: Basic Science, Medical devices, Medical Ethics, Neuroscience/Mental Health, Science and Medicine, Science and the Media

Leave a Comment (33) ↓

33 thoughts on “Science by press release: A helmet to fight Alzheimer’s disease?

  1. PalMD says:

    These guys should be ashamed of themselves, unless they are too stupid to understand what they are doing.

    To market a treatment to hopeless people, without any real evidence of efficacy is so immoral that it boggles the mind.

  2. David Gorski says:

    I don’t think they’re marketing it to patients yet. They appear to be marketing it to investors; my guess is that they’re looking for venture capitalists to pony up to help the fund their R&D and the costs of getting regulatory approval for this device.

    I still think it’s an ethically highly dubious tactic, though, to go to the press in this way on such thin evidence. I understand that devices are designed on speculative science, but before having some real evidence of efficacy they’re hyping it as though it’s the cure for Alzheimer’s disease.

  3. qetzal says:

    If Dougal was quoted accurately, I think it’s well beyond dubious. It’s plain unethical:

    Currently all you can do with dementia is to slow down the rate of decay – this new process will not only stop that rate of decay but partially reverse it.

    Not “I think” or “we hope,” but “this…will.”

    Making such a claim would be unethical even with reams of mouse data from multiple labs and a positive double blind pilot human study. To claim that based on one mouse study and an unblinded, uncontrolled study in 6 patients is absolutely unethical.

    IF Dougal was quoted accurately (and this is far from certain), he deserves to be strongly reprimanded by Durham U’s ethical oversight body.

  4. mjranum says:

    But, but, but, butbutbutbut! They are wearing lab coats – they must be real scientists! You can’t wear a lab coat unless you’re a real scientist, right?

    Those appear to be $4 computer fans they have hot-glued to the helmet. I guess that’s to cool the LEDs? Oh, wait, LEDs don’t get hot.

  5. The alternate hypothesis is that this is a media misadventure, rather than a calculated deception to raise research funds. Scientists who are not media savvy often fall prey to an overly eager press office or reporter.

    It could also be a little of both – the researchers wanted some press attention to garner attention and funding, but it got out of their control and the end result was much more than they anticipated.

    I will attempt to contact them to get their input, but they may be overwhelmed right now.

  6. mjranum says:

    It’s got all the hallmarks of woo-woo. Most revealing, to me, is that they are reaching for general panacea status. You know – it could reverse all aging. Yeah. Right.

    And the “scientist” didn’t say that his tests on himself were double-blinded. That tells me either that he’s an idiot or he’s a conman – but in either case he’s no scientist.

  7. David Gorski says:

    I will attempt to contact them to get their input, but they may be overwhelmed right now.

    That’d make a fine followup post.

    I would have contacted them myself, but I only first carefully read the links sent to me by readers over the weekend. Also, I had originally planned to do a post on a different subject; however, the more I thought about it, the more I decided that this topic was timely and deserved a quick commentary. However, it was only early evening yesterday when I decided to do a post on it. (Yes, I’m a notorious procrastinator.) I spent a couple of hours going over the paper and the literature and refreshing my memory about NIR spectroscopy by looking up some literature I had on it, and then I wrote.

    I would say, however, that some of the statements made by Dougal and Haslam, unless taken way out of context, tend to argue against a press office misadventure. “Will not only stop that rate of decay but partially reverse it”? “We could be able to affect and change the rate at which our bodies age”? “Enhance the immune system”? “Treat viral meningitis”? Come on! That’s not the sort of stuff that careful scientists say without a lot of caveats and qualifications tacked on. In any case, I never accused Dougal and company of a “calculated deception to raise funds,” merely of being way premature in going to the press with this research in such a big way.

  8. DBonez says:

    When I see press-based science releases, I worry about the legitimacy of the claim, but I also worry about unscrupulous woo-woo promoters copying the device and marketing it based solely on the initial research hypothesis.

    LEDs do get hot. High-power LED arrays, commonly available through many US sources, and extremely prevalent in Chinese electronics markets, are becoming common-place in many lighting applications. Because they consume several watts of power and are still only in the range of 15-20% efficient, they require heatsinks or fan cooling to prevent excess heat and to extend the array’s operating life.

    As an electronics engineer with some medical training, I can quickly read the press release and look at and reverse-engineer the Alzheimer helmet and determine that in all likelihood, it’s several groups of high-power LED arrays with fans to cool them. If I can do this, many others can too.

    All it will take is a little financing, a little advertizing, and some engineering and copies of these devices could be entering the US by the container load and becoming a billion-dollar market making wild claims of cures and miracles. The woo-woo marketers will cite the original study and sell many of these copied devices to grief stricken, desperate families with the glimmer of hope that it will “cure” their debilitated loved ones. Even if the original study ends up completely refuted and disproven scientifically, which I doubt, the CAM market will already be off-and-running and many will profit greatly from the unknowing and unsuspecting followers of alternative/integrative medicine. And, once the seed of possibility is planted, the theory of operation will become “societal medical fact” that it works. After that happens, no amount of research will be able to erase the memories of the believers and any attempt to ague the efficacy will lead to conspiracy claims and contempt for the medical research community. We’ve seen this many times before.

    I would love to see followups to this post and see where it goes. I fear I already know where is may go.

  9. daedalus2u says:

    If I may suggest a mechanism.

    The paper on NIR photodissociation of “poisons” from cytochrome c oxidase is likely the basis.

    Normally cytochrome c oxidase is tonally inhibited by NO, which blocks O2 from binding and is the major regulatory pathway by which mitochondria regulate their O2 consumption.

    With NO blocking cytochrome c oxidase, the electron respiration chain becomes fully reduced and O2 can pick up electrons from complex III, forming superoxide. This superoxide is vectorally produced in the inner matrix, where MnSOD dismutates it at near diffusion controlled kinetics. NO also reacts with superoxide at near diffusion controlled kinetics and it is the destruction of NO by superoxide generated by too great a reduction of the respiration chain that lowers the NO level and disinhibits cytochrome c oxidase so that O2 can consume electrons (and be reduced to water).

    If this light does dissociate NO from cytochrome c oxidase it would cause the respiration chain to become more oxidized and would reduce the quantity of superoxide formed. This would increase NO levels and upregulate ATP levels via sGC.

    This might work in the short term for people who already have low ATP. I would be very concerned how it modifies the normal regulatory pathway(s) by which the number of mitochondria per neuron is regulated. My research indicates that regulation involves formation of long lived NOx species which accumulate in mitochondria and which release NO during autophagy and then trigger appropriate mitochondria biogenesis. I think those long lived NOx species include nitrated proteins, which derive only from the combination of NO and superoxide. The formation of superoxide by mitochondria under metabolic “stress” is the signal by which the cell “measures” the metabolic stress of the mitochondria it has, and then infers how many it needs to make. In a neuron that number can be different by 3 or more orders of magnitude depending on the length of the axons.

    In the rat CNS, mitochondria lifetime is on the order of a month.

    If this is working by some physiological mechanism (other than the placebo effect), then it could have serious side effects. It might slow the progression of Alzheimer’s for a while by operating existing mitochondria in a way that generates less superoxide. But if that compromises the regulation of mitochondria number, the progression could greatly accelerate at some future time when mitochondria wear out faster than they are replaced.

    Cytochrome c oxidase is not the only heme enzyme inhibited by NO. All the cytochrome P450 enzyme are too. Many of them are active in the brain. How is changing the operating point of all of those enzymes going to change things? Very complexly, and very likely not in only benign ways.

  10. Simon says:

    daedalus2u: Interesting idea- It’s been a while since I studied biochem so excuse me if this is a silly response but:

    a) Alzheimers (in my limited knowledge of the subject) does not have the hallmarks of a metabolic disease caused by low ATP. The plaques are physical entities which I assume are produced from amyloid created by the cells, a metabolic process. I would imagine low ATP to create conduction problems and maybe dying brain cells, but I’d be surprised by the plaques. Like I said though, my knowledge on the subject is old and weak.
    b) Are we assuming that the skull and other superficial tissues are transparent to this wavelength of NIR? Has that been studied?

    Just my two cents. Oh and also, daedalus, please don’t take this as an attack as I do respect you and your knowledge, but I think as skeptics we should aim to keep the tone of our discussions accessible to people both within and without the biological sciences- in other words, would you mind reposting your mechanism (or a summary) with limited technobabble for non-biochemsits and lapsed ones such as myself!

  11. Blake Stacey says:

    Those appear to be $4 computer fans they have hot-glued to the helmet. I guess that’s to cool the LEDs? Oh, wait, LEDs don’t get hot.

    As DBonez pointed out, LEDs sure do get hot — particularly if they’re bright enough to be really fun. Not only can they get warm, they can bring a whole new meaning to the phrase, “She blinded me with science!”

  12. daedalus2u says:

    One of the most consistent symptoms of Alzheimer’s is a reduction in brain metabolism. Amyloid (and all the other protein aggregates of the neurodegenerative disorders) is normally cleared by ATP powered proteases in the proteasome, or during autophagy (which requires an ATP powered pH gradient). My hypothesis of Alzheimer’s is that the buildup of amyloid is a natural compensatory mechanism to cope with there being not enough ATP. There are simply more important things to use ATP for (when there is not enough) than to use it to get rid of amyloid (or to make new mitochondria). If the ATP setpoint is too low, my hypothesis is that ATP conservation pathways are invoked (which include not getting rid of amyloid) as in ischemic preconditioning. I discuss this in my blog on fevers and autism 1/1/08. Getting rid of garbage is something that can always be put off “a little bit longer” if there is something better to do. I think that Alzheimer’s happens when that heuristic is taken a bit too far.

    Nerve conduction is a lot more important than getting rid of amyloid. If your nerves are not conducting properly, a bear could catch and eat you. Keeping nerves alive is too. Amyloid buildup causes essentially no problems for quite a while, months, even years. My mother and both her parents died with advanced Alzheimer’s, so I am not being flip, I know what it can do. But that the brain can function so well and for so long with such a serious decline in metabolism is quite remarkable to me. One of the things that has helped me in my research is that I inherited my mother’s low nitric oxide physiology, so I experienced quite dramatic changes when I corrected it (I appreciate that my experiences are anecdotes).

    I will try and re-express the light idea with less technicalese, not sure how well it will come across. I think I only have two modes of communication, very terse and highly technical, and very long and only a little less technical but with all the details.

  13. durvit says:

    My first thought on seeing the headlines and the infra-red was that it was going to be some form of reprise of an infra-red detoxing idea (very common) but, thanks to your explanation, I now see that that was way offbeam (no pun intended).

    Science by press-release in tabloids or such is becoming surprisingly common in the UK. Recently, Prof Holford and Smith have announced the value of B vitamins for lowering homocysteine levels and the risk of Alzheimer’s Disease; they chose to do this in the Daily Record. Within the last few days, that renowned journal, The Leamington Chronicle broke the news of a groundbreaking treatment for autism.

    If this continues, I’m expecting the next genomic medicine breakthrough to be announced in a My Little Pony fanzine.

  14. BlazingDragon says:

    Sigh. This sounds like psuedoscience. It has just enough plausibility to be true…

    I agree with DBonez’s assessment of where this will go. In liberal political circles, ideas like these are called “zombie memes” (no matter how often you kill the idea with facts, it magically resurrects itself in a few days, weeks, or months, as strong as if you’d never killed it 1000 times over with facts and logic).

    I really do hope the the authors did get caught up by an over-enthusiastic (or unethical) reporter, but I fear this isn’t the case. I’ll be very interested to see the follow-ups on this.

    P.S. A giant-screen TV in Japan, composed entirely of LEDs, needs its own gigantic refrigeration unit to keep from burning out in a matter of minutes. High-power LEDs can get scalding-hot and need to be cooled to give them a useful lifetime. Of course, we have no idea of the power usage of this helmet, but the fans are theoretically necessary. As far as I know, bio-luminescence is the only truly “cool” form of light, and I’ve yet to see a high-power, high-intensity application of it. Now if I could just get the picture out of my head of super-bright fireflies bursting into flames…

  15. neurocritic says:

    I think these particular authors are trying to jump on the Alzheimer’s “miracle cure” bandwagon rolled out by the Tobinick and Gross press release:

    “Reversal Of Alzheimer’s Symptoms Within Minutes In Human Study

    ScienceDaily (Jan. 9, 2008) — An extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer’s disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation.

    . . .

    “The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept…”

    Even though the finding was published, the actual article reads like physician’s notes, not a research study or clinical trial. Here’s the extent of their “immediate effect” (with absolutely no placebo condition, of course):

    “Ten minutes after dosing the patient was reexamined. He was noticeably calmer, less frustrated, and more attentive. He was able to correctly identify the state as California, and he identified the year as 2006. His responses to questioning seemed less effortful and more rapid, with less latency. He left for author HG’s office for further testing.”

    So the magic helmet folks didn’t want to be left behind…

  16. daedalus2u says:

    If they got results in only 4 weeks, it can’t be anything that takes longer than that to happen. I presume that growth of new neurons and connecting them in the “right” places would take longer than that.

    If this does do “something”, what is the correct dose and how does that dose get determined, and is that dose the same for every individual?

  17. Chris Noble says:

    I have to admit that my second thought was wrong, mainly because I somehow neglected to notice the “near” in front of the “infrared.” This makes a difference.

    I wouldn’t be so quick. Unless they can provide a mechanism by which electromagnetic radiation of this wavelength is supposed to interact with molecules in the brain then it is a very reasonable assumption that the only thing that is going on is heating.

    Are they proposing some sort of resonant absorption?

  18. Chris Noble says:

    Q. How can a light heal my Cold Sore?
    We believe that the 1072nm light acts as a catalyst, which enhances the local immune response, which enables the body to heal itself more rapidly.

    Light acts as a catalyst? WTF is this supposed to mean?

    Q. Will any light do as long as I put it on my cold sore?
    No, over the last 10 years Virulite has been researching the various wavelengths (colours) of light in the visible and invisible spectrum and found some wavelengths were ineffective and some even make Cold Sores worse! Only 1072nm light proved to be effective in reducing Cold Sore healing time

    Only 1072nm light? The same wavelength that cures Alzheimer’s with no side effects?

  19. Simon says:

    daedalus, thank you for your response, I understand your mechanism far better now. I also understand it to the degree where I know I cannot comment on its validity so I’ll leave that to the biochemists. Don’t worry too much about the jargonese- I enjoy reading things on a technical level too, I was just hoping that a rewording could allow others to appreciate your comments too.

  20. David Gorski says:

    I wouldn’t be so quick. Unless they can provide a mechanism by which electromagnetic radiation of this wavelength is supposed to interact with molecules in the brain then it is a very reasonable assumption that the only thing that is going on is heating.

    Yes and no. Work that I found on wound healing and cultured cells suggests that the mechanism is more specific than just heating. Also, NIR can penetrate the skull; otherwise NIR imaging of cerebral blood flow would be impossible. Granted NIR imaging only “sees” the surface of the brain, only penetrating an inch or so, but it can penetrate the skull.

    That being said, I’m beginning to think that I might have been too easy on these guys. The more I read, the more I come to think that the scientific mechanism is implausible at best. It might work, but I think the odds are pretty low, and without a lot more data in mice at least I’m not convinced.

  21. daedalus2u says:

    A figure that shows the mitochondria respiration chain and how that fits with my idea of how the magic light helmet works is here

    If this NIR light does do “something”, I suspect it would be via modulation of kinetics of either free radical reactions, decay of “excited transition states” in activated molecules, or in photodissociation of things from other things (such as NO from cytochrome c oxidase). There could easily be hundreds of things that are being affected, none of which are well understood.

    If it does any of those things it is likely to do so indiscriminately. There is nothing “magic” about 1072 nM, these investigators looked at a handful of wavelengths (where LEDs are available for cheap). Something like that might have a short term positive effect but is very likely to be very bad in the longer term. Physiology is too complex and too coupled to simply whack away at it indiscriminately and make it “better”.

    The paper linked to is about nitration of proteins in mitochondria as part of the normal regulation of those mitochondria. That regulation is very complex, occurs over a great many different time scales and under quite different physiological conditions (and in different tissue compartments). There is very little understanding of how it is functioning under “normal” conditions. How it functions under conditions of variable and intermittent exposure to light of 1072 nM is completely unknown. From what these investigators have written, it would appear that they are not even aware enough to ask these questions.

    A (poor) analogy would be to suppose that one had a car with 100,000 miles on it, and it is starting to run not as well as it used to. A salesman says he can “fix” the car by installing nitrous oxide injection and by adding nitromethane to the fuel. Sure enough when you do that, the car “runs” better than it ever has. But if the car had been nursed along gently, it could have easily gone 150,000 miles, but with nitromethane it only goes 100,500. That is why long term trials with the proper endpoints (i.e. death) are most appropriate for terminal conditions like Alzheimer’s. Four weeks is too short. I imagine that the right dose of cocaine or amphetamine might produce “improvement” in Alzheimer’s for 4 weeks but would accelerate decline and hasten death.

  22. jayh says:

    A couple of questions come to mind.

    1) A mouse skull is VASTLY thinner than a human skull, a mouse brain is vastly smaller, i.e. radiation that would penetrate through a mouse skull and brain would barely reach the outer layer of a human brain. Goosing up the power would seem to provide lots of scalp burns, and would heat the outer part of the brain significantly trying to treat the inner part.

    2) NIR is abundant in sunlight. Why doesn’t walking around in the sun provice the same miraculous effect?

  23. Ted Powell says:

    After reading this article and comments yesterday morning, I went to the Daily Mail article. There were just four comments posted, all generally accepting:
    “Sounds like an amazing breakthrough…”
    “I wonder if NICE will approve this treatment…”
    “Let’s hope that this works…”
    “I’m very interested…”

    I left a brief comment with the URL of this article, and got a page saying that it would be sent to a moderator. So far, there are still only the same four comments there…

  24. daedalus2u says:

    neurocritic, the paper on the acute improvement in Alzheimer’s on injection of Etanercept in the spine is available online.

    The authors suggest an effect in synapses. I consider that unlikely. I think an NO explanation fits better. Higher NO does cause long term potentiation and would likely be very rapid (seconds).

    Etanercept blocks the TNF alpha receptor. TNFa down regulates the expression of eNOS.

    Etanercept treatment reduces the production of superoxide in aged blood vessels.

    The very rapid resolution of symptoms of neurological disorders is not unprecedented. The paper on the acute resolution of autistic symptoms with fever shows similar changes. An acute fever is a high NO state due to expression of iNOS. NO is one of the fundamental neurotransmitters that among other things regulates long term potentiation and long term depression. “Fever therapy” (actual induction of malaria) was the “standard of care” for treating neurosyphilis for decades before penicillin was available. In some cases mental acuity was restored very rapidly (~1 day). I go into a lot of the NO related details in my blog. Neurosyphilis is characterized by some of the same symptoms as Alzheimer’s, brain inflammation and white matter hyperintensities. I think for the same reasons.

    I think this very rapid improvement is consistent with NO being what regulates the functional connectivity of the brain in real time. I think that is what the BOLD (blood O2 level dependant) signal is. NO is released by nNOS, that consumes O2 and produces a slight dip in O2 levels, a high NO level is produced which diffuses into a volume, activates sGC causing vasodilation which increases local blood flow increasing O2 levels (that is where the increased O2 comes from), O2Hb is the sink for NO, the erythrocytes take up the NO and carry it away, the vessels constrict and the O2 level goes back to baseline. I think this is how the brain metaprograms itself, via releasing NO in the brain region where it needs stuff to get done.

    I am blogging my ideas of what the physiology behind the Magic Light Helmet.

  25. daedalus2u says:

    I just found a paper which discusses the effect of NIR on mitochondria. They used liver cell mitochondria and found cytochrome c release.

    This is a serious and even deadly problem for neurons. Cytochrome c is only coded for by nuclear DNA. Every time a little bit is lost, there is no way to replace it other than by turning over the mitochondria via autophagy and mitochondria biogenesis. This only occurs in the cell body. It cannot occur in axons far from the cell body.

    It occurs to me that this might be a factor in ALS, in particular the “flail arm variant”. (I wonder if Dr. Novella would care to comment?)

    ALS is associated with exposure to sunlight. Presumably the only light that matters is light that the tissues are transparent to, and which reaches the motor neurons. In general, the arms are more exposed to light than the legs due to coverings and the orientation of legs is usually vertical while the arms are not.

    If the Magic Light Helmet is causing cytochrome c release in the brain, the brain could fail catastrophically when the mitochondria loose too much and can’t be replace fast enough or transported out to the tippy ends of the axons fast enough.

    At the very least they should do periodic MRIs to see if this is happening. There would probably be decreased diffusion (white matter hyperintensities) as the ATP supply goes down.

  26. apteryx says:

    daedalus2u – I’m intrigued by your hypotheses regarding the silly helmet, which are mostly over my head as this isn’t my area of expertise, but what is your basis for saying that ALS is correlated with sunlight exposure? I do not find any support for this in searching PubMed, nor in a quick consultation of our society’s ultimate references (Wikipedia and Google). OTOH, lack of the exposure to sunlight which we have evolved to experience may be connected to subclinical vitamin D deficiency and a number of illnesses more common than ALS.

  27. daedalus2u says:

    There have been reports of excess ALS in agricultural workers.

    People have tried to associate the agricultural excess with exposure to agricultural “chemicals”, but those results have been mixed. I would think exposure to an environmental chemical agent would affect the arms and legs equally. In the flail arm variant the arms are affected first even though the arm motor neurons are shorter than in the legs. The only exposure I can really think of that could symmetrically affect arms more than legs would be exposure to light. If it was muscle activity arms should be affected asymmetrically because arm use is asymmetric.

    There does seem to be a lower incidence in non-Caucasians. If it were only due to short wavelength light, the incidence in dark skinned people would be very low (the way that skin cancer is). The skin is more transparent to near infrared radiation where melanin has lower absorbance.

    The association with mutant SOD has been shown to not be due to a loss of SOD activity, but rather due to some unknown gain in function, so the attribution to oxidative stress from sunlight likely isn’t correct. All the mSOD variants do have less stability, particularly in the metal free form and tend to form misfolded agglomerates more. That is similar to the gain in function of the mutant protein implicated in Huntington’s disease, the formation of protein aggregates and similar to what is observed in Alzheimer’s, accumulation of amyloid. One gain in function in ALS and Huntington’s might be to increase ATP demand to turn over these protein aggregates. Disposal of damaged proteins requires ATP either in the proteasome or during autophagy. Oxidative stress would upregulate SOD expression, but wouldn’t be the ultimate “cause” (usually oxidative stress is secondary to something else). Oxidative stress is observed in ALS, but I think that is secondary to insufficient mitochondria.

    My research includes work on the short term regulation of ATP and long term regulation of mitochondria number. Both of these are regulated by NO. Low NO increases ATP production rate, but at the expense of ATP concentration and eventually mitochondria biogenesis (but at different time scales). I suspect that there is some dysregulation of both in ALS. An acute increase in ATP demand (to clear aggregated proteins) might lead to decreased mitochondria biogenesis over time. Because motor neurons are one of the largest cells with the most mitochondria, they are likely quite sensitive to any imbalance between mitochondria lifetime and mitochondria biogenesis. Once you get into a situation of insufficient mitochondria, a low NO state is invoked to increase ATP production from the remaining mitochondria. If the NO level ever becomes low enough to impede mitochondria biogenesis, there is no way for physiology to recover.

    Thinking about the Magic Light Helmet opened up some new ideas for me associated with cytochrome c release after seeing the paper I link to above. There is some interaction between SOD and cytochrome c in mitochondria. That might be part of the mSOD link to ALS.

    If light is a trigger for ALS, it would likely have a pretty clear threshold. The exposure would have to be “enough” to trigger the transition to a low NO hypermetabolic state in the motor neurons. That can only occur over (about) the lifetime of mitochondria.

    If this is the mechanism for the Magic Light Helmet (rather than placebo), then it is shortening mitochondria lifetime. I will be writing that up in more detail and posting it on my blog. I am now pretty sure that is the mechanism for the positive effects observed in the Alzheimer’s patients. I think people without Alzheimer’s might experience increased mental acuity too. However, if my hypothesis is correct this will lead to insufficient mitochondria and will induce an irreversible neurodegeneration over time. That time may not be long, less than a year (but the timing is highly uncertain). Once it starts to happen there will likely be no way to reverse it, even in the previously healthy people. At that point, increased use of the Magic Light Helmet may reverse symptoms briefly (a day or so), but will exacerbate them over all longer time frames. The effect would be analogous to “tolerance” exhibited by some drugs where the level for therapeutic effects increases over time and can exceed the toxic level.

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