Research Paper|Volume 8, Issue 6|pp 1250—1258

Reversal of cognitive decline in Alzheimer's disease

Dale E. E. Bredesen^1,², Edwin C. C. Amos³, Jonathan Canick⁴, Mary Ackerley⁵, Cyrus Raji⁶, Milan Fiala⁷, Jamila Ahdidan⁸

¹Easton Laboratories for Neurodegenerative Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095, USA
²Buck Institute for Research on Aging, Novato, CA 94945, USA
³Department of Neurology, University of California, Los Angeles, CA 90095, USA
⁴Memory Clinic, California Pacific Medical Center, San Francisco, CA 94115, USA
⁵Private Practice of Psychiatry, Tucson, AZ 85718, USA
⁶Department of Radiology, University of California, Los Angeles, CA 90095, USA
⁷Department of Surgery, University of California, Los Angeles, CA 90095, USA
⁸Brainreader, Horsens, Denmark

Received: April 12, 2016Accepted: May 30, 2016Published: June 12, 2016

https://doi.org/10.18632/aging.100981

Copyright: © 2016 Bredesen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published [1]. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4−, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.