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), where he began investigating the effects of Transcranial Electromagnetic Treatment (TEMT) on brain pathology and cognitive function in AD transgenic mice.  AD is characterized by the production and 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.

Examination of the brains from AD mice in these multiple studies clearly showed that TEMT reversed brain Aβ aggregation – a mechanism that appears central to the cognitive benefits observed in the same AD 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).

Aβ oligomers form over 6 days in control brain tissue from AD mice (left). However, TEMT prevents this Aβ oligomer formationwhen givenover thesame period (right).

Aβ oligomers form over 6 days in control brain tissue from AD mice (left).
However, TEMT prevents this Aβ oligomer formation when given over the same period (right).

Growing evidence indicates that the small Aβ oligomers inside neurons are a primary cause of neuronal dysfunction and death in AD. In that regard, NeuroEM Therapeutics TEMT technology is unique in being the only AD therapeutic shown to prevent and reverse Aβ aggregation both inside and outside neurons. To our knowledge, no drug currently being developed has this critical ability. Importantly, no deleterious effects of daily TEMT (for up to 8 months) were evident in brain or body of treated AD mice, based on multiple histologic, neurochemical, and blood markers evaluated.

TEMT Prevents and Treats AD by blocking and reversing Aβ aggregation.

TEMT Prevents and Treats AD by blocking and reversing Aβ aggregation.

Following their initial 2010 paper, Dr. Arendash and colleagues published five additional 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 have 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 – well before memory impairment is noticed. NeuroEM Therapeutics’ most recent basic science research (sponsored by NIH) has indicated the ability of TEMT to dissociate other toxic proteins in the brain besides Aβ.

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 hundreds of thousands of 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 Therapeutics’ Phase I clinical trial in AD patients was approved in early 2016 by the Western Institutional Review Board (WIRB). The WIRB also designated the company’s MemoEM 1000 head device being used in that trial as a Non-Significant Risk device. This pioneering clinical trial (recently completed), was the first clinical study involving long-term administration of TEMT to the entire human brain. Public disclosure of the results from this Phase I clinical trial will occur shortly. The design and details of the 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”.


Since 2010, Dr. Gary Arendash (CEO and President) and seven collaborating laboratories have published six peer-reviewed papers in first tier scientific journals detailing the effects of TEMT on behavior, neuropathology, and physiologic processes in AD mice. These papers are listed below. Because Dr. Arendash’s 2012 and 2016 review articles summarize work from the prior papers, they can be conveniently downloaded directly from this web page. Also listed below is the partial title and authors of the manuscript submitted for publication that details results from NeuroEM’s Phase I clinical trial.


  • 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, Submitted for Publication.

  • 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, in press. 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. 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, 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, 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, 2010.


Clinical Collaborators

NeuroEM Therapeutics’ Phase I clinical trial was performed at the University of South Florida’s Byrd Alzheimer’s Institute in Tampa, FL. The Byrd Institute is the largest free-standing Alzheimer’s Institute in the world and has a large staff of experienced Alzheimer’s clinicians/researchers. The Principle Investigator for this first-of-its-kind clinical trial was Dr. Amanda Smith, Director of Clinical Trials at the Institute.  NeuroEM Therapeutics was most pleased to have the Byrd Institute doing this trial, particularly since its clinicians are committed to exploring promising approaches against Alzheimer’s Disease beyond standard Big Pharma-sponsored drug trials.

Product Development Timeline

NeuroEM Therapeutics has an aggressive clinic-to-market timeline of 3+ years. This timeline depends on fund availability and results of upcoming clinical trials.


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, 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.

As the TEMT head devices are further refined, extensive technical data is being collected for the filing of additional non-provisional patents, with the objective of building a substantial patent portfolio around the technology and devices – both in the U.S. and internationally. Along that line, NeuroEM submitted two CIPs to their 2014 non-provisional application, as well as two PCT’s for international coverage in February 2019. All four applications have claims related to the technical/operational aspects of the company’s TEMT head devices.