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 by David Gorski

Dr. Gorski's full information can be found here, along with information for patients. David H. Gorski, MD, PhD, FACS is a surgical oncologist at the Barbara Ann Karmanos Cancer Institute specializing in breast cancer surgery, where he also serves as the American College of Surgeons Committee on Cancer Liaison Physician as well as an Associate Professor of Surgery and member of the faculty of the Graduate Program in Cancer Biology at Wayne State University. If you are a potential patient and found this page through a Google search, please check out Dr. Gorski's biographical information, disclaimers regarding his writings, and notice to patients here.