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:
1NeuroEM Therapeutics, Inc., Phoenix, AZ, USA.
2College of Pharmacy, University of South Florida, Tampa, FL, USA.
3University of South Florida Health/Byrd Alzheimer's Institute, Tampa, FL, USA.
4Left Coast Engineering, Escondido, CA, USA.
5Invicro, Boston, MA, USA.
6School of Aging Studies, University of South Florida, Tampa, FL, USA.
7Department of Neurology, 2nd Faculty of Medicine, Charles University/Motol University Hospital, Prague, Czech Republic.
8Ocotillo Electromagnetics, Inc., Chandler, AZ, USA.
9RF Exposure Laboratory, San Marcos, CA, USA.
10University 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
