Evidence map›Paper›PMID 23249780›Full record

ArticleClinical pharmacology and therapeutics2013

Using genetics to enable studies on the prevention of Alzheimer's disease.

D G Crenshaw, W K Gottschalk, M W Lutz, I Grossman, A M Saunders, J R Burke, K A Welsh-Bohmer, S K Brannan, D K Burns, A D Roses

Abstract read
In one paragraph

Article in Clinical pharmacology and therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–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.

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

40 citing papers in PubMed.

  1. bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Genes · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. The effects of the TOMM40 poly-T alleles on Alzheimer's disease phenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2018
    Review
  13. Article
  14. Neuropathologic features of TOMM40 '523 variant on late-life cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2017
    Article
  15. Article
  16. Characterization ofAlzheimer's & dementia (New York, N. Y.) · 2017
    Article
  17. Article
  18. Proteomic differences in brain vessels of Alzheimer's disease mice: Normalization by PPARγ agonist pioglitazone.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  19. Neurology · 2017
    Article
  20. Article
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

10 authors.

D G CrenshawJoseph & Kathleen Bryan Alzheimer's Disease Research Center, Department of Neurology, Duke University Medical Center, Durham, North Carolina, USA.
W K Gottschalk
M W Lutz
I Grossman
A M Saunders
J R Burke
K A Welsh-Bohmer
S K Brannan
D K Burns
A D Roses

Funding

NEUROPATHOLOGY COREP30AG028377 · NIA · DUKE UNIVERSITY · PI WELSH-BOHMER, KATHLEEN ANNE · 2006 to 2011
$9.6M
NIA NIH HHS NIA P30AG-028377NIA NIH HHS P30 AG028377
6 · The paper itself

Abstract

Curing Alzheimer's disease (AD) remains an elusive goal; indeed, it may even prove to be impossible, given the nature of the disease. Although modulating disease progression is an attractive target and will alleviate the burden of the most severe stages, this strategy will not reduce the prevalence of the disease itself. Preventing or (as described in this article) delaying the onset of cognitive impairment and AD will provide the greatest benefit to individuals and society by pushing the onset of disease into the later years of life. Because of the high variability in the age of onset of the disease, AD prevention studies that do not stratify participants by age-dependent disease risk will be operationally challenging, being large in size and of long duration. We present a composite genetic biomarker to stratify disease risk so as to facilitate clinical studies in high-risk populations. In addition, we discuss the rationale for the use of pioglitazone to delay the onset of AD in individuals at high risk.

Indexed as

AgedAged, 80 and overAge FactorsAlzheimer DiseaseBiomarkersCognitionDisease ProgressionGenetic Predisposition to DiseaseHumansHypoglycemic AgentsPioglitazoneRandomized Controlled Trials as TopicRisk FactorsThiazolidinedionesTime FactorsBiomarkersHypoglycemic AgentsPioglitazoneThiazolidinediones

Identifiers

PMID23249780
PMCPMC4131283

What OpenQuestion holds

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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.