Can Transcranial Electromagnetic Treatment Turn the Tide in Alzheimer Disease?


The founder and CEO of NeuroEM Therapeutics discussed the potential of transcranial electromagnetic treatment and shared insight into the advantages it may hold over the traditional treatment route.

Dr Gary Arendash

Gary Arendash, PhD, founder and CEO, NeuroEM Therapeutics

Gary Arendash, PhD

A recent trial of transcranial electromagnetic treatment (TEMT) has suggested that the investigational treatment for Alzheimer disease may induce clinically important and significant improvements in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) scores.

After showing these apparent "disease-modifying" actions both prevent and reverse memory impairment in Alzheimer transgenic mice, the treatment was assessed in 8 patients with mild-to-moderate Alzheimer. As well as the aforementioned improvements, increases were seen in cognition-related changes in CSF oligomeric amyloid-beta (Aβ), cerebrospinal fluid (CSF) levels of soluble Aβ1-40 and Aβ1-42, and a decreased CSF p-tau/Aβ1-42 ratio, and reduced levels of oligomeric Aβ in plasma in adult humans.

Gary Arendash, PhD, founder and CEO, NeuroEM Therapeutics, a Phoenix-based medical device company developing the intervention, told NeurologyLive that it may be able to reverse cognitive impairment. He also shared more about what’s next for TEMT on the regulatory path and insight into how it works.

NeurologyLive: What’s the next step for transcranial electromagnetic treatment toward regulatory approval?

Gary Arendash, PhD: In medical devices, you don't need thousands of patients when doing a final trial. the pivotal trial that I'm talking about, generally, is the combination phase 2/3 trial if we were doing a drug. But for a medical device, it is the single trial, and we have done already some power analyses and we will, of course, consult with our FDA consultants.

To see how many patients are so happy with it and have that actually be the protocol—that they would be happy with it when the results turn out. I think that puts us be in a good position for the FDA to approve our device, as perhaps the first effective treatment against Alzheimer's disease.

For those who are unfamiliar, could you provide some background on the device and its advantages?

Basically, the device is a double-layered cap, like an EEG. Embedded in between the 2 layers are 8 emitters for the electromagnetic treatment to go into the brain—1 emitter for each of the 4 lobes on each side of the brain. These emitters are connected by a cable to a control box and a battery that the patient wears on their arm, so this allows really near complete mobility for patients to do whatever they would like in-home. Obviously, don't take a shower during treatments. In this particular study, it was 1 hour in the morning, 1 hour in the late afternoon, so twice a day, but future studies—especially longer future studies—may not require both periods in any given day. The device is easy to wear, and it's administered by the caregiver. The caregiver charges the device, turns it on, positions the cap, does all of that, and it really a wonderful in-home device where you're getting 120 treatments in 2 months, and you don't have to go to the clinic 120 times.

Could you expand on how the electromagnetic treatment process works?

As far as what exactly the electromagnetic fields do to provide these behavioral benefits, the blood and the cerebral spinal fluid changes in Alzheimer markers, those look really quite beneficial. Where a lot of Alzheimer's researchers are coming from today as far as what root causes of Alzheimer's are involve 2 toxic proteins. One is called beta amyloid (Aß) and the other is tau. The neurons make both of these proteins which, unfortunately, have a natural tendency to self-aggregate. These individual monomeric Aß aggregate with one another. There may be 2, 5, 7, 8, 21—and collectively, these are called oligomers. Aß oligomers, in and of themselves, can be toxic and are toxic to a number of cellular processes. Just as important is that they initiate the other toxic protein to aggregate. The bottom line is that you have to toxic oligomers floating around, soluble oligomers in neurons, and they cause the dysfunction.

The electromagnetic waves have no problem penetrating from the scalp, through the cranium into the brain, into the brain’s neurons, and to disaggregate these 2 types of toxic oligomers. The reason that we feel that is happening is that these oligomers are that the individual units are held together by hydrogen bonds, which are relatively weak. The electromagnetic waves actually cause a vibration or a resonance rotational motion, whichever way you want to look at it, and this eventually weakens these bonds, therefore disaggregating the toxic protein into its individual, innocuous single units.

What challenges might this treatment address?

The problem with all these drugs that have failed—and there's about 140 or 150 right now—is that, first of all, they have difficulty getting into the brain, in the blood-brain barrier and then into neurons. Even if they got through the blood-brain barrier and into the neurons, it’s insignificant amounts. They do not have the capacity to attack and be specific for these aggregates, these 2 different toxic aggregates. They do not target Aß oligomers or tau oligomers, and you've got the target both of them. It's not drugs that can do that right now, and so that's why we feel that this medical device has a real chance to not just slow the disease down or to stabilize it—as my colleagues in Big Pharma would be happy with—but to actually reverse the disease process. In animal model studies, if you can get rid of these toxic oligomers of Aß and tau, you get a reversal of the important cellular processes—repaired mitochondrial function, reoccurred microtubule polymerization—and we think that that is a part of why we're getting these reversal effects in such a short period of time, 2 months in the Alzheimer patients.

I disagree with most of my colleagues in Alzheimer research who believe that, always, by the time you're diagnosed with Alzheimer, it's too late and there's nothing that can be done about this disease. We've got to go earlier on, in terms of more the preventative phase and even the pre-symptomatic phase and start treating patients then. I disagree respectfully. I think that the reason why drugs have not worked against people who are diagnosed with the disease is that they're not getting into the brain, into the neurons, and they do not have the ability to attack those oligomers that electromagnetic waves disaggregate.

Transcript edited for clarity.


Arendash G, Cao C, Abulaban H, et al. A clinical trial of transcranial electromagnetic treatment in Alzheimer’s disease: Cognitive enhancement and associated changes in cerebrospinal fluid, blood, and brain imaging. J Alzheimers Dis. Published online August 6, 2019. doi: 10.3233/JAD-190367.

Related Videos
Michael Levy, MD, PhD
Michael Kaplitt, MD, PhD
Michael Kaplitt, MD, PhD
video 4 - "Amyloid Cascade Hypothesis of Alzheimer’s Disease"
Video 3 - "Amyloid Precursor Protein and Amyloid Beta Species in Alzheimer’s Disease"
Svetlana Blitshteyn, MD, FAAN, director and founder of Dysautonomia Clinic
© 2024 MJH Life Sciences

All rights reserved.