A Clinical Trial of Transcranial Electromagnetic Treatment in Alzheimer's Disease: Cognitive Enhancement and Associated Changes in Cerebrospinal Fluid, Blood, and Brain Imaging.


Author: Arendash G1, Cao C2, Abulaban H3, Baranowski R4, Wisniewski G5, Becerra L5, Andel R6,7, Lin X2, Zhang X2, Wittwer D8, Moulton J9, Arrington J10, Smith A3

Affiliation: <sup>1</sup>NeuroEM Therapeutics, Inc., Phoenix, AZ, USA.

<sup>2</sup>College of Pharmacy, University of South Florida, Tampa, FL, USA.

<sup>3</sup>University of South Florida Health/Byrd Alzheimer's Institute, Tampa, FL, USA.

<sup>4</sup>Left Coast Engineering, Escondido, CA, USA.

<sup>5</sup>Invicro, Boston, MA, USA.

<sup>6</sup>School of Aging Studies, University of South Florida, Tampa, FL, USA.

<sup>7</sup>Department of Neurology, 2nd Faculty of Medicine, Charles University/Motol University Hospital, Prague, Czech Republic.

<sup>8</sup>Ocotillo Electromagnetics, Inc., Chandler, AZ, USA.

<sup>9</sup>RF Exposure Laboratory, San Marcos, CA, USA.

<sup>10</sup>University Diagnostic Institute, Tampa, FL, USA.
Conference/Journal: J Alzheimers Dis.
Date published: 2019 Aug 6
Other:
  Special Notes: doi: 10.3233/JAD-190367. [Epub ahead of print]   ,  Word Count: 284  
    BACKGROUND: Small aggregates (oligomers) of the toxic proteins amyloid-β (Aβ) and phospho-tau (p-tau) are essential contributors to Alzheimer's disease (AD). In mouse models for AD or human AD brain extracts, Transcranial Electromagnetic Treatment (TEMT) disaggregates both Aβ and p-tau oligomers, and induces brain mitochondrial enhancement. These apparent "disease-modifying" actions of TEMT both prevent and reverse memory impairment in AD transgenic mice.



OBJECTIVE: To evaluate the safety and initial clinical efficacy of TEMT against AD, a comprehensive open-label clinical trial was performed.



METHODS: Eight mild/moderate AD patients were treated with TEMT in-home by their caregivers for 2 months utilizing a unique head device. TEMT was given for two 1-hour periods each day, with subjects primarily evaluated at baseline, end-of-treatment, and 2 weeks following treatment completion.



RESULTS: No deleterious behavioral effects, discomfort, or physiologic changes resulted from 2 months of TEMT, as well as no evidence of tumor or microhemorrhage induction. TEMT induced clinically important and statistically significant improvements in ADAS-cog, as well as in the Rey AVLT. TEMT also produced increases in cerebrospinal fluid (CSF) levels of soluble Aβ1-40 and Aβ1-42, cognition-related changes in CSF oligomeric Aβ, a decreased CSF p-tau/Aβ1-42 ratio, and reduced levels of oligomeric Aβ in plasma. Pre- versus post-treatment FDG-PET brain scans revealed stable cerebral glucose utilization, with several subjects exhibiting enhanced glucose utilization. Evaluation of diffusion tensor imaging (fractional anisotropy) scans in individual subjects provided support for TEMT-induced increases in functional connectivity within the cognitively-important cingulate cortex/cingulum.



CONCLUSION: TEMT administration to AD subjects appears to be safe, while providing cognitive enhancement, changes to CSF/blood AD markers, and evidence of stable/enhanced brain connectivity.



KEYWORDS: Amyloid-β; FDG-PET; brain electromagnetic waves; cognitive enhancement; functional MRI



PMID: 31403948  DOI: 10.3233/JAD-190367