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

NeuroEM’s Co-Founder and Chief Executive Officer, Dr. Gary Arendash, was Research Professor at the University of South Florida (USF) and the Florida Alzheimer’s Disease Research Center 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.


All of NeuroEM’s clinical studies have administered TEMT to Alzheimer’s (AD) patients using our first-of-its-kind and patented medical device, the MemorEMTM.  This device was deemed a “non-significant risk” device by the Western Institutional Review Board and FDA has bestowed its first “breakthrough” designation against AD to the MemorEM device and NeuroEM’s TEMT technology.

The MemorEM™ 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 already completed clinical trials. 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 our initial 2-month period of daily TEMT or during a total of 18 months of daily TEMT over a 2½ year 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/Functional Performance

In an initial Pilot clinical trial involving eight mild/moderate AD subjects, twice daily 1-hour TEMT was provided in-home for two months by caregivers.  Following this treatment period, a reversal of cognitive impairment was observed for 7 of 8 subjects in ADAS-cog and for all 8 subjects in Rey AVLT (Figure 3).  The combination of our extensive pre-clinical studies and this initial clinical study’s cognitive findings resulted in FDA providing “Breakthrough” designation for TEMT technology and the MemorEM device against AD in 2020 — the first drug or device receiving that designation.

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

Because of the promising results from the aforementioned initial clinical study, and the enthusiasm of the study’s AD patients/caregivers to continue treatment, 4-month and 12-month extension studies were performed, with breaks of 8- and 5-months interposed with no treatment (31 months total).  Despite the two lengthy periods of no treatment, daily in-home TEMT was able to safely stop otherwise certain cognitive decline over a 2½ year period in all six cognitive/functional tasks individually, as well as in an overall “composite” cognitive analysis.  Moreover, caregiver assessments throughout that 2½ year period indicate no change in Global Deterioration Scale (GDS) stage of AD – in other words, the caregivers felt their AD subjects had not declined in cognitive/functional abilities over a 2½ year period.   Most non-treated AD subjects would have substantially declined in memory and in their ability to perform daily activities of living over this extended treatment period.

Our clinical cognitive results strongly argue for initiation of a placebo-controlled, larger clinical trial with TEMT to treat established AD.  As such, a Phase IIb/III (Pivotal) clinical trial is anticipated to be initiated later this year.

AD Markers in Brain and Blood

Long-term TEMT through 14-27 months induced changes in, or modulated, major AD markers in both CSF and plasma, suggesting that TEMT has effects on the actual AD pathogenic process.  In CSF, long-term TEMT induced reductions in levels of C-reactive protein, p-tau217, Aβ1-40, and Aβ1-42, while modulating CSF oligomeric Aβ levels.  In plasma, long-term TEMT modulated/rebalanced levels of both p-tau217 and total tau.  These TEMT-induced effects on AD markers were evident many months after the start of treatment and may have contributed to the stoppage of cognitive/functional decline over a 2½ year period in the same AD subjects.

Immune Regulation/Rebalancing in Brain and Blood

For the eight mild/moderate AD subjects in our initial 2-month treatment study, we sought to determine if their TEMT administration had immunologic effects on blood or CSF levels of 12 cytokines.  For 8 plasma cytokines, AD subjects with lower baseline cytokine levels always showed increases in those cytokines after 2-months of daily TEMT.  By contrast, those AD subjects with higher baseline cytokine levels in plasma showed treatment-induced decreases in plasma cytokines.  Thus, a gravitation to reported normal plasma cytokine levels (i.e., a “rebalancing”) occurred with both acute and long-term TEMT.  Figure 4 shows this TEMT-induced rebalancing of IL-17α and IL-18 in plasma to near normal levels.

Figure 4: As is evident for both plasma IL-17α and IL-18, the response to TEMT is dependent on baseline levels, with TEMT inducing convergence (rebalancing) toward aged normal levels (horizontal dashed line).


In the CSF, TEMT-induced a similar rebalancing for seven measurable cytokines, the direction and extent of changes in individual subjects also being linked to their baseline CSF levels.  Our results strongly suggest that daily TEMT to AD subjects for 2-months can “rebalance” levels for 11 of 12 cytokines in blood and/or brain, which is associated with reversal of their cognitive impairment.  This rebalancing of so many cytokines, and in both brain and systemic compartments, appears to be a remarkable new mechanism of TEMT action that may contribute substantially to it’s potential to stop or reverse AD and other diseases of aging

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

Clinical Study Conclusions:

  • TEMT administration to AD subjects was safe, while providing cognitive enhancement, changes to AD markers in CSF/blood, immune regulation, 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 and 9 collaborating laboratories have published/submitted 10 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 of them, except for the 2022 manuscript currently submitted for publication, can be downloaded by clicking on their purple underline.


  • 2022

    Arendash, G., Abulaban, H., Steen, S., Andel, R., Wang, Y., Bai, Y, Baranowski, R., McGarity, J., Scritsmier, L., Lin, X, Shen, N, Aljassabi, A., Li, Y, and C. Cao.  Transcranial Electromagnetic Treatment Stops Alzheimer’s Disease Cognitive Decline Over a 2½ Year Period: A Pilot Study.  Medicines, Vol. 9, August 3, 2022. TEMT Stops AD Memory Decline 


    Cao, C., Abulaban, H., Baranowski, R., Wang, Y., Bai, I., Lin, X., Shen, N, Zhang, X., and G. Arendash.  Transcranial Electromagnetic Treatment “Rebalances” Blood and Brain Cytokine Levels in Alzheimer’s Patients: A New Mechanism for Reversal of Their Cognitive Impairment.  Frontiers in Aging Neuroscience 14: Article 829049, 2022. TEMT rebalances cytokines 

  • 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.


NeuroEM has a well-defined path to commercialization, having already completed a Pilot clinical trial and two extension clinical trials that demonstrate safety and initial efficacy.  NeuroEM now anticipates initiation of its Phase IIb/III Pivotal clinical trial in Fall of 2022.  This will be a double-blind controlled trial which, if successful, will form the basis for an application to FDA of its MemorEMTM device to stop and reverse Alzheimer’s cognitive decline.  The company currently has a Series “A” funding round in progress, primarily to fund the first component of its Phase IIb/III Pivotal trial.  NeuroEM has worked closely with FDA in the design of this trial and has the strong support of the National Institute on Aging (NIA) as one of its funded, featured companies.  NeuroEM is open to exploring strategic partnerships with established companies offering collaborative support, including strategic funding. The company anticipates that the first therapeutic to stop/reverse AD (its MemorEM device) could be available for commercialization as early as late 2025. 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.


NeuroEM has three issued U.S. patents (either directly or through exclusive license) and twelve submitted patent applications.  Many of Dr. Arendash’s initial findings provided the basis for a patent application filed through the University of South Florida, which was then licensed to NeuroEM in 2013 through an exclusive worldwide licensing agreement.  The USPTO issued the patent in 2016 (U.S. patent 9,238,149 B2) covering the technology Dr. Arendash and colleagues developed while at USF. The major claim of this patent is that TEMT can prevent or reverse the cognitive dysfunction and associated neuropathology of AD and other amyloid-based neurologic disorders.  A CIP was filed by USF in 2015 and issued in 2018 (U.S. patent 10,149,982), which further extends the utility of TEMT, providing further coverage for use of TEMT against many neurologic conditions, and broadens the range of TEMT treatment parameters.  NeuroEM’s own issued patent (U.S. patent 10,765,879) provides protection for the company’s MemorEM devices, particularly regarding the range of various treatment parameters and use in numerous other neurologic diseases/disorders.

 The Company’s twelve patent applications (six PCTs, and six U.S. applications) have been filed by NeuroEM in 2019 through 2021.  They further describe the functionality and capabilities of the MemorEM device, extend the disorders treatable by TEMT, and cover additional technical/operational aspects of the MemorEM head device.

Collectively, these patents/applications provide NeuroEM with substantial and expanding IP coverage for our TEMT technology, which should protect NeuroEM as the only company legally able to market TEMT against a variety of neurologic disorders in the U.S. and (via PCTs) internationally.