Propagating electromagnetic waves, showing their inter-digitated electrical (red) and magnetic (blue) components.

In 2008, NeuroEM’s Founder and Chief Executive Officer, Dr. Gary Arendash was at the University of South Florida (USF), when he began investigating the effects of Transcranial Electromagnetic Treatment (TEMT) on brain pathology and cognitive function in AD transgenic mice with his USF colleague Dr. Chuanhai Cao. AD appears to be initiated by the aggregation of an abnormal brain protein called β-amyloid (Aβ) during aging. AD transgenic mice are genetically-engineered so that their neurons have the same human gene that produces human Aβ. Once produced, this human Aβ protein then aggregates inside and outside neurons in their brains to start the AD disease process, just as in humans.

In such AD mice, it was found that TEMT begun early in adulthood (before AD neuropathology and cognitive impairment occurs) protected AD transgenic mice from otherwise certain cognitive impairment. If TEMT was delayed until old age (when extensive neuropathology and cognitive impairment were present), TEMT reversed both the Aβ protein aggregation and the cognitive impairment of these old AD transgenic mice. This anti-Aβ aggregating effect of TEMT occurred both outside neurons (reducing the size of large Aβ deposits) and inside neurons (reducing small Aβ oligomers). Growing evidence indicates that these small Aβ oligomers inside neurons are the primary initiator of neuronal dysfunction and death in AD. Importantly, no deleterious effects of daily TEMT (for up to 8 months) were evident in brain or body of treated AD mice.

Following their initial 2010 paper, Dr. Arendash and colleagues published five additional pre-clinical papers that further underscore the utility of TEMT in AD transgenic mice to enhance cognitive function and reduce brain AD neuropathology. These follow-up papers identified two additional mechanisms of action that work in concert with the anti-Aβ aggregation mechanism initially identified – namely, mitochondrial enhancement (to increase energy production in neurons) and increased neuronal activity in brain regions impacted by AD. These additional mechanisms are important because brain mitochondrial dysfunction and decreased neuronal activity occur very early in the AD process – before memory impairment is noticed. NeuroEM Therapeutics’ most recent basic science research (supported by NIH SBIR grant 1R43NS90653-01A1) has indicated the ability of TEMT to not only prevent Aβ aggregation, but to also prevent p-tau aggregation, in human AD brain tissue (see below figure; purple cylinders represent either Aβ or p-tau). This is important because Aβ aggregation induces p-tau aggregation, both of which then appear to cause the neuronal dysfunction and death of AD. Thus, TEMT dissociates both of the toxic proteins currently thought to be at the root cause of AD. To our knowledge, no drug currently being developed has this critical ability.

TEMT can block or reverse aggregation of both Aβ and p-tau

Mounting evidence indicates that disaggregation of Aβ and p-tau oligomers by TEMT occurs through a destabilization of the relatively week hydrogen-bonds between oligomer monomers through dipole-dipole inter-actions, vibration, and/or resonance phenomena. In this regard, electromagnetic/radiofrequency waves in the range used in our studies have been shown to cause reduced dipole-dipole interactions (dielectric loss), which leads to a decrease in inter-molecular hydrogen-bonding. Indeed, the toxic protein β-sheet aggregates of Aβ and tau have a common backbone polarization that is stabilized via “two-electron” interactions of hydrogen bonds – a backbone that appears to be selectively disrupted by the radiofrequency waves we utilized

TEMT technology is similar in a number of ways to the electromagnetic waves generated by cell phones. Numerous studies in normal humans have shown that such exposure can provide beneficial cognitive changes to the EEG, increases brain energy production, and has no deleterious effects on health over many years. Moreover, recent epidemiologic studies involving over a million subjects have all concluded that electromagnetic exposure to the brain (via cell phones) for 15-20 years does not increase the risk of any form of cancer, including brain gliomas.


NeuroEM’s recently-completed clinical trial (CLICK HERE TO DOWNLOAD) is the first to administer TEMT to the entire human brain, and over an extended period of time. This pilot study was designed to evaluate the safety and initial clinical efficacy of TEMT against AD. Eight mild/moderate AD patients were treated with TEMT in-home by their caregivers for two months utilizing NeuroEM’s MemorEM™ head device. TEMT was given for two 1-hour periods each day, with subjects primarily evaluated at baseline, end-of-treatment (2M), and 2-weeks following treatment completion. The design and details of this clinical trial can be viewed by going to and entering the indicator number “NCT 02958930” into the search window or by typing in “Alzheimer’s, electromagnetic”.

The MemorEM™ head device is self-contained and has been designed for in-home daily treatment, allowing for complete mobility and comfort in performing daily activities during treatment (Figure 1A). The device has a custom printed circuit board (control panel) that is powered by a rechargeable battery. This control panel/battery box is worn on the upper arm and wired via a cable to eight (8) uniquely bioengineered emitters embedded between a double-layered head cap worn by the subject. (Figure 1B). The MemorEM device shown below is NeuroEM’s Generation One (Gen1) device used in the company’s now-published pilot study. NeuroEM has recently developed a Gen2 device with higher power and compliance-monitoring capabilities. The Gen2 device will be used in future clinical trials, including NeuroEM’s up-coming Pivotal trial.

Figure 1: The MemorEM™ Head Device

Human head computer simulations performed by NeuroEM show that the 8 emitters collectively provide both global and penetrating TEMT exposure to the human forebrain, including the cerebral cortex and underlying structures (Figure 2). The below figure of computerized simulations shows the electric field penetration from each emitter when on. Importantly, only one emitter is active at any given time, with rapid sequential activation of all 8 antennas over 200 times per second. Similar brain penetration results were seen utilizing a human head phantom in actual electromagnetic lab testing.

Figure 2: TEMT penetration into the brain


No deleterious side effects/behaviors were reported by the subjects or their caregivers during the 2-month treatment period. As well, no significant changes in blood pressure or temperature occurred during treatment sessions, and no abnormalities were observed in post-treatment MRI scans (e.g., no tumors, no new micro-hemorrhages) – all suggesting that global brain TEMT is a safe therapeutic in AD subjects at current parameters and study duration.

Cognitive Performance

A comprehensive battery of cognitive tasks was administered at baseline, at end of treatment (Day 60), and 14-days following completion of treatment. Multiple measures of memory were improved by the end of the 2-month treatment period compared to baseline performance. In the benchmark cognitive task used in AD therapeutic trials (ADAS-cog), averaged memory performance was improved by over 4 points for seven of the 8 AD patients (Figure 3, left). This benefit, which was highly “clinically significant” (Effect Size of 1.21), was maintained even two weeks after TEMT administration had stopped. In a second major task of memory performance, the Rey AVLT, very large “clinically significant” effects were observed in 5-Trail recall, and maintained two weeks after treatment (Figure 3, right). Based on these encouraging cognitive benefits and the subjects’ collective enthusiasm to continue treatment, an extension study ( Protocol NCT03927040) is now in progress providing these same AD subjects with TEMT over a 29 month period following the initial 2-months of treatment (31 months total treatment period). Based on these encouraging cognitive benefits and the subjects’ collective enthusiasm to continue treatment, two extension studies have now been completed ( Protocols NCT02958930 and NCT03927040), which have provided these same AD subjects with over 2 1/2 years of treatment.  Although there were two breaks in treatment and the number of subjects is small, NeuroEM now has clear evidence that TEMT can stop/stabilize AD memory loss for over 2 1/2 years – a period over which non-treated AD subjects would have substantially declined in memory and in their ability to perform daily activities of living.

Figure 3: TEMT Enhances Memory in ADAS-cog and AVLT

Cerebrospinal Fluid (CSF) and Blood Analysis.

CSF is the fluid circulating within and around the brain. It is often referred to as a “window into the brain” because CSF reflects what is happening chemically in the brain. Soluble Aβ1-40 and Aβ1-42 (the two major forms of Aβ) in CSF are almost totally non-aggregated (single unit) Aβ. Compared to baseline, both of these AD markers in CSF were increased following the 2-month treatment period (Figure 4A and B). This is consistent with TEMT breaking up Aβ oligomers in the brain and the resulting single unit Aβ diffusing into the CSF. Also consistent with TEMT breaking up Aβ oligomers in the brain were the significantly lower levels of Aβ oligomers in blood (plasma) after 2-months of TEMT treatment, which was even maintained two weeks afterwards (Figure 4C). These results suggest that TEMT had affected the disease process in AD patients.

Figure 4: TEMT increases soluble Aβ in CSF and decreases oligomeric Aβ in plasma

Brain Imaging Analysis.

Fractional Anisotropy (FA) is a measure of “functional” brain MRI that is widely used to evaluate functional connectivity (communication) between neurons in the brain. Multiple studies have shown that brain FA consistently decreases as AD progresses (i.e., less neuronal communication). This decrease in FA occurs even over periods as short as three months in AD patients, and particularly in a brain area critical for memory integration called the cingulate cortex/cingulum. Our FA brain imaging focused on the cingulate cortex/cingulum and found that, in addition to the expected regional decreases in FA within this brain area, two months of TEMT resulted in regional enhancements in FA for all subjects. Figure 5 shows the FA pattern observed for one subject – red/orange/yellow pixels indicate increased FA following TEMT; blue pixels indicate the expected decrease in FA. These regional FA increases seen in the cingulate cortex/cingulum of AD patients following 2-months of TEMT suggest greater functional connectivity/communication, which may have contributed to the improved memory shown by these AD patients.

Figure 5: Increased functional connectivity (red, orange, yellow) in Cingulum following TEMT

Study Limitations:

  • All subjects received treatment without inclusion of an untreated/placebo group
  • There were a relatively small number of AD subjects (eight) in this study
  • Although 120 treatments were given, the 2-month treatment period was relatively short

Clinical Study Conclusions:

  • TEMT administration to AD subjects was safe, while providing cognitive enhancement, changes to AD markers in CSF/blood, and evidence of enhanced brain functionality.
  • TEMT appears to be “disease-modifying” against AD, is non-invasive, and easily administered in-home.
  • Although these promising results need to be replicated in controlled clinical trials, they suggest that TEMT may provide a vertical leap to an entirely new bioengineering-based intervention against Alzheimer’s Disease.


Since 2010, Dr. Gary Arendash (CEO and Founder) and seven collaborating laboratories have published seven peer-reviewed papers in first tier scientific journals detailing the effects of TEMT on behavior, neuropathology, and physiologic processes in AD mice and human AD patients. All of these papers are listed below. Each one of them, including NeuroEM’s just-published 2019 paper of clinical trial results, can be downloaded by clicking on their purple underline.


  • 2019

    Arendash, G., Cao, C., Abulaban, H., Baranowski, R., Wisniewski, G., Becerra, L., Andel, R., Lin, X., Zhang X., Wittwer, D., Moulton, J., Arrington, J., and A. Smith. A Clinical Trial of Transcranial Electromagnetic Treatment in Alzheimer’s Disease: Cognitive Enhancement and Associated Changes in CSF, Blood, and Brain Imaging. Journal of Alzheimer’s Disease, Vol 71: 57-82. TEMT Clinical Trial in AD Patients

  • 2016

    Arendash, G.W. Review of the Evidence that Transcranial Electromagnetic Treatment (TEMT) will be Safe and Effective Against Alzheimer’s Disease. Journal of Alzheimer’s Disease 53: 753-71, http://dx.doi: 10.3233/JAD-160165, 2016.
    EMF Review in JAD

  • 2012

    Arendash, G.W. Transcranial Electromagnetic treatment (TEMT) for Alzheimer’s Disease: Why it has the potential to trump Alzheimer’s drug development. Journal of Alzheimer’s Disease 32:243-266, 2012. Publication
    EMF Review in JAD.

  • 2012

    Arendash G.W., Mori, T., Dorsey, M., Gonzalez, R., Tajiri, N., and C. Borlongan. Long-Term 918 MHz Electromagnetic Field Treatment to Very Old Alzheimer’s Mice Reverses β-Amyloid Deposition, Modifies Regional Cerebral Blood Flow, & Provides Selected Cognitive Enhancement without Brain Hyperthermia. PLoS ONE Publication, 2012.

  • 2011

    Mori, T. and G.W. Arendash. Electromagnetic field treatment enhances neuronal activity: Linkage to cognitive benefit and therapeutic implications for Alzheimer’s Disease. Journal of Alzheimer’s Disease and Parkinsonism Vol. 1:102, 2011.

  • 2011

    Dragicevic, N., Bradshaw, P.C., Mamcarz, M., Lin, X., Wang, L., Cao, C., and G.W. Arendash. Long-term electromagnetic field treatment enhances brain mitochondrial function of both Alzheimer’s transgenic mice and normal mice: A mechanism for electromagnetic field-induced cognitive benefit? Neuroscience 185: 135-149, http://dx.doi: 10.1111/j.1600-079X.2011.00864.x, 2011.

  • 2010

    Arendash., G.W., Sanchez-Ramos. J., Mori, T., Mamcarz, M., Lin, X., Runfeldt, M., Wang, L., Zhang, G., Sava, V., Jun Tan, J., and C. Cao Electromagnetic Field Treatment Protects Against and Reverses Cognitive Impairment in Alzheimer’s Mice. Journal of Alzheimer’s Disease 19: 191-210, http://dx.doi: 10.3233/JAD-2010-1228, 2010.


Operational, clinical, and basic science funding has thus far been attained largely from NIH (NINDS, NIA), angel investors, family offices, and private investors. NeuroEM’s MemorEM™ head device and associated pilot clinical trial were reviewed by the FDA, which had no concerns of safety/design. The Western Institutional Review Board (WIRB) then designated both as “Non-Significant Risk (NSR)”. NeuroEM will begin a controlled Pre-Pivotal clinical trial soon, with a large Pivotal trial anticipated to begin in mid-2022. The company currently has a Series “A” funding round in progress, primarily to fund the Pre-Pivotal clinical trial. NeuroEM is working closely with FDA in the design of the Pre- Pivotal and Pivotal trials which, if successful will result in NeuroEM requesting FDA approval for its Gen2 MemorEM device to treat the cognitive impairment of Alzheimer’s Disease. NeuroEM is open to exploring a strategic partnership with an established company offering marketing collaboration &/or strategic funding. The company anticipates that the first medical device for treating AD (its MemorEM device) could be available for commercialization as early as 2024. Following FDA approval of the device, expedited availability of the device to the public via payers (i.e., Medicare) should occur in view of the company’s “Breakthrough Device” Designation by FDA and its close working relationship with FDA.


In 2013, NeuroEM Therapeutics signed an exclusive worldwide license agreement with the University of South Florida (USF) for use of their recently issued U.S. patent (US 9,238,149 B2) and the technology developed by Gary Arendash, Ph.D while he was at USF. The major claims of this patent are that TEMT can prevent and reverse the cognitive dysfunction in Alzheimer’s Disease and other neurologic conditions involving Aβ aggregation. A follow-up CIP, filed in 2015, was issued in December 2018 (US 10,149,982 B2). This CIP further expanded on the neurologic conditions treatable with TEMT and the parameters utilized therein.

In addition, NeuroEM Therapeutics submitted a non-provisional patent application (US 2014/0257017 A1), published in 2014 and issued in 2020, that describes a self-contained head device for administration of electromagnetic treatment against a spectrum of neurologic conditions. In 2016, NeuroEM Therapeutics entered into an exclusive license agreement with Remarkable Technologies (Connecticut) involving their patent (US 9,238,149 B2) for a parallel application of electromagnetic technology into a head device.

Along with the aforementioned four issued patents/licenses, NeuroEM has filed seven patent applications since early 2019 – four in the U.S. and three internationally. These applications have claims resulting from the extensive technical data collected from both the Gen1 and Gen2 MemorEM devices. The company is building a substantial patent portfolio around its technology and devices – both in the U.S. and internationally.