Evidence map›Paper›PMID 27294343›Full record

ArticleAging2016

Reversal of cognitive decline in Alzheimer's disease.

Dale E Bredesen, Edwin C Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, Jamila Ahdidan

Registry-linked trialAbstract read
In one paragraph

Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05894954 (EVANTHEA TRIAL), which is not on this map. Cited by 71 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05894954 phase3completednot on this mapstarted 2023, after this paper: background citation

EVANTHEA TRIAL: A Pragmatic, Randomized, Controlled Trial to Evaluate the Effectiveness of a Precision Medicine Treatment Approach for Early Dementia and Mild Cognitive Impairment

TypeinterventionalSponsorAlzheimer's Prevention and Reversal Project, Inc.Ran2023 to 2026Enrolled73ConditionsMild Cognitive Impairment, Dementia, MildArmsPrecision Medicine Approach, Hormones and Medications tailored to lab tests, combined with devices that support stress management and brain exercises, Standard-of-Care, Lifestyle including diet, exercise, stress management
3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  15. Restore Health: Disease Reversal.Family medicine · 2026
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Dale E BredesenEaston Laboratories for Neurodegenerative Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095, USA.
Edwin C AmosDepartment of Neurology, University of California, Los Angeles, CA 90095, USA.
Jonathan CanickMemory Clinic, California Pacific Medical Center, San Francisco, CA 94115, USA.
Mary AckerleyPrivate Practice of Psychiatry, Tucson, AZ 85718, USA.
Cyrus RajiDepartment of Radiology, University of California, Los Angeles, CA 90095, USA.
Milan FialaDepartment of Surgery, University of California, Los Angeles, CA 90095, USA.
Jamila AhdidanBrainreader, Horsens, Denmark.

Funding

UCLA ALZHEIMERS DISEASE RESEARCH CENTERP50AG016570 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CUMMINGS, JEFFREY L. · 1999 to 2014
$25.9M
Novel Prionic Mechanism Underlying Alzheimer?s DiseaseR01AG034427 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BREDESEN, DALE E. · 2009 to 2012
$1.5M
APP signaling networkR21AG036975 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BREDESEN, DALE E. · 2012 to 2013
$520k
NIA NIH HHS P50 AG016570NIA NIH HHS R01 AG034427NIA NIH HHS R21 AG036975
6 · The paper itself

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.

Indexed as

AgedAlzheimer DiseaseApolipoprotein E4BrainCognitive DysfunctionDisease ProgressionFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedNeuropsychological TestsOrgan SizeRecovery of FunctionTreatment OutcomeApolipoprotein E4Alzheimer's diseaseApolipoprotein Ebiomarkerscognitiondementiaimagingneurodegenerationneuropsychology

Identifiers

PMID27294343
PMCPMC4931830

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.