Evidence map›Paper›PMID 25324467›Full record

Trial reportAging2014

Reversal of cognitive decline: a novel therapeutic program.

Dale E Bredesen

Registry-linked trialAbstract readCase ReportsClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Aging, 2014. 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 85 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 3 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

85 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. American journal of Alzheimer's disease and other dementias
    Trial
  7. Article
  8. Review
  9. Review
  10. Restore Health: Disease Reversal.Family medicine · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Neuroglia in cognitive reserve.Molecular psychiatry · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

25 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

1 author.

Dale E BredesenMary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095. Buck Institute for Research on Aging, Novato, CA 94945.

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 AG034427NIA NIH HHS AG036975NIA NIH HHS AG16570NIA NIH HHS P50 AG016570NIA NIH HHS R01 AG034427NIA NIH HHS R21 AG036975
6 · The paper itself

Abstract

This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer's disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND). The first 10 patients who have utilized this program include patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI). Nine of the 10 displayed subjective or objective improvement in cognition beginning within 3-6 months, with the one failure being a patient with very late stage AD. Six of the patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. Improvements have been sustained, and at this time the longest patient follow-up is two and one-half years from initial treatment, with sustained and marked improvement. These results suggest that a larger, more extensive trial of this therapeutic program is warranted. The results also suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes. Furthermore, given the failure of monotherapeutics in AD to date, the results raise the possibility that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system.

Indexed as

AgedAlzheimer DiseaseCognitive DysfunctionFemaleHumansMaleMiddle Aged

Identifiers

PMID25324467
PMCPMC4221920

What OpenQuestion holds

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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 OpenQuestion graph.