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Aging (Albany NY). 2016 Jun;8(6):1250-8. doi: 10.18632/aging.100981.

Reversal of cognitive decline in Alzheimer's disease.

Author information

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

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.

KEYWORDS:

Alzheimer's disease; Apolipoprotein E; biomarkers; cognition; dementia; imaging; neurodegeneration; neuropsychology

PMID:
27294343
PMCID:
PMC4931830
DOI:
10.18632/aging.100981
[Indexed for MEDLINE]
Free PMC Article

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