Evidence map›Paper›PMID 19519301›Full record

ReviewCurrent Alzheimer research2009

A common biological mechanism in cancer and Alzheimer's disease?

M I Behrens, C Lendon, C M Roe

Open access · greenAbstract readReview
In one paragraph

Review in Current Alzheimer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 3 pooled it
8.6field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 3 syntheses or guidelines pooled it, 185 citations in OpenAlex.

  1. Inverse relationship between cancer and Alzheimer's disease: a systemic review meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
    Pooled it
  2. Alzheimer disease and cancer risk: a meta-analysis.Journal of cancer research and clinical oncology · 2015
    Pooled it
  3. Pooled it
  4. Accumulation of amyloid beta in human glioblastomas.Clinical and experimental immunology · 2020
    Trial
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40 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

3 authors at 2 institutions in 1 country.

M I BehrensDepartamento de Neurología y Neurocirugía, Hospital Clínico Universidad de Chile and Clínica Alemana Santiago, Chile. mbehrens@redclinicauchile.cl
C Lendon
C M Roe
University of Chile · CLClínica Alemana · CL

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI Tammie Lee Smith Benzinger · 1985 to 2026
$69.5M
WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
NIA NIH HHS P01 AG003991NIA NIH HHS P50 AG005681
6 · The paper itself

Abstract

Cancer and Alzheimer's disease (AD) are two common disorders for which the final pathophysiological mechanism is not yet clearly defined. In a prospective longitudinal study we have previously shown an inverse association between AD and cancer, such that the rate of developing cancer in general with time was significantly slower in participants with AD, while participants with a history of cancer had a slower rate of developing AD. In cancer, cell regulation mechanisms are disrupted with augmentation of cell survival and/or proliferation, whereas conversely, AD is associated with increased neuronal death, either caused by, or concomitant with, beta amyloid (Abeta) and tau deposition. The possibility that perturbations of mechanisms involved in cell survival/death regulation could be involved in both disorders is discussed. Genetic polymorphisms, DNA methylation or other mechanisms that induce changes in activity of molecules with key roles in determining the decision to "repair and live"- or "die" could be involved in the pathogenesis of the two disorders. As examples, the role of p53, Pin1 and the Wnt signaling pathway are discussed as potential candidates that, speculatively, may explain inverse associations between AD and cancer.

Indexed as

Alzheimer DiseaseNeoplasmsAgingAmyloid beta-PeptidesAnimalsCell CycleHumansModels, BiologicalSignal TransductionTumor Suppressor ProteinsWnt ProteinsAmyloid beta-PeptidesTumor Suppressor ProteinsWnt Proteins

Identifiers

PMID19519301
PMCPMC2810550
OpenAlexW2170197381

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.