Evidence map›Paper›PMID 29071250›Full record

ArticleThe journal of prevention of Alzheimer's disease2017

Defining Disease Modifying Therapy for Alzheimer's Disease.

J Cummings, N Fox

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The journal of prevention of Alzheimer's disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 3 pooled it
5.3field-weighted citation impact, top 4% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

  1. Pooled it
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  4. Trial
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  8. Article
  9. Article
  10. What should convince a clinician of disease modification in Alzheimer's disease clinical trials?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  11. Article
  12. Review
  13. Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

26 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

2 authors at 2 institutions in 2 countries.

J CummingsCleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV, USA.
N FoxDementia Research Centre, Department of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, United Kingdom.
Lou Ruvo Brain Institute · USUniversity College London · GB

Funding

Renewal of Centers of Biomedical Research Excellence (COBRE) (Phase 2) CNTN - ResubmissionP20GM109025 · NIGMS · CLEVELAND CLINIC FOUNDATION · PI JESSICA KIRKLAND CALDWELL · 2015 to 2026
$22.8M
NIGMS NIH HHS P20 GM109025The Dunhill Medical Trust R337/0214
6 · The paper itself

Abstract

backgroundDisease-modifying therapies (DMTs) are urgently needed to treat the growing number of individuals with Alzheimer's disease (AD) or at immanent risk for AD. A definition of DMT is required to facilitate the process of DMT drug development. PROCESS: This is a review of the state of the science with regard to definition and development of DMTs.

resultsA DMT is as an intervention that produces an enduring change in the clinical progression of AD by interfering in the underlying pathophysiological mechanisms of the disease process that lead to cell death. Demonstration of DMT efficacy is garnered through clinical trial designs and biomarkers. Evidence of disease modification in the drug development process is based on trial designs such as staggered start and delayed withdrawal showing an enduring effect on disease course or on combined clinical outcomes and correlated biomarker evidence of an effect on the underlying pathophysiological processes of the disease. Analytic approaches such as showing change in slope of cognitive decline, increasing drug-placebo difference over time, and delay of disease milestones are not conclusive by themselves but support the presence of a disease modifying effect. Neuroprotection is a related concept whose demonstration depends on substantiating disease modification. No single type of evidence in itself is sufficient to prove disease modification - consistency, robustness, and variety of sources of data will all contribute to convincing stakeholders that an agent is a DMT.

conclusionDMT is defined by its enduring effect on processes leading to cell death. A variety of types of data can be used to support the hypothesis that disease modification has occurred.

Indexed as

Alzheimer’s diseaseamyloidbiomarkerdisease modifying therapystaggered start

Identifiers

PMID29071250
PMCPMC5653310
OpenAlexW2892067140

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.