Evidence map›Paper›PMID 19647374›Full record

ArticleMedical hypotheses2009

The X-chromosome instability phenotype in Alzheimer's disease: a clinical sign of accelerating aging?

Vladan P Bajić, Biljana Spremo-Potparević, Lada Zivković, David J Bonda, Sandra L Siedlak, Gemma Casadesus, Hyoung-Gon Lee, Mark A Smith

Open access · bronzeAbstract read
In one paragraph

Article in Medical hypotheses, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Melatonin and abeta, macular degeneration and alzheimers disease: same disease, different outcomes?Medical hypothesis, discovery & innovation ophthalmology journal · 2012
    Article
  11. Cell cycle deregulation in the neurons of Alzheimer's disease.Results and problems in cell differentiation · 2011
    Review
  12. Review: cell cycle aberrations and neurodegeneration.Neuropathology and applied neurobiology · 2010
    Review
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

8 authors at 3 institutions in 2 countries.

Vladan P BajićInstitute of Biomedical Research, Galenika ad, 11000 Belgrade, Serbia. vladanbajic@yahoo.com
Biljana Spremo-Potparević
Lada Zivković
David J Bonda
Sandra L Siedlak
Gemma Casadesus
Hyoung-Gon Lee
Mark A Smith
Case Western Reserve University · USUniversity of Belgrade · RSInstitute of Agricultural Economics Belgrade · RS

Funding

Role of Cell Cycle in NeurodegenerationR01AG028679 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LEE, HYOUNG-GON · 2008 to 2012
$1.6M
Cell Cycle Inhibitors in Alzheimer DiseaseR21AG031364 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI SMITH, MARK A · 2007 to 2008
$357k
NIA NIH HHS AG028679NIA NIH HHS AG031364NIA NIH HHS R01 AG028679NIA NIH HHS R21 AG031364
6 · The paper itself

Abstract

Premature centromere division, or premature centromere separation (PCS), occurs when chromatid separation is dysfunctional, occurring earlier than usual during the interphase stage of mitosis. This phenomenon, seen in Robert's syndrome and various cancers, has also been documented in peripheral as well as neuronal cells of Alzheimer's disease (AD). In the latter instances, fluorescent in situ hybridization (FISH), applied to the centromere region of the X-chromosome in interphase nuclei of lymphocytes from peripheral blood in AD patients, demonstrated premature chromosomal separation before mitotic metaphase directly after completion of DNA replication in G(2) phase of the cell cycle. Furthermore, and perhaps unexpectedly given the presumptive post-mitotic status of terminally differentiated neurons, neurons in AD patients also showed significantly increased levels of PCS of the X-chromosome. Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelerated aging of the affected brain.

Indexed as

Chromosomal InstabilityChromosomes, Human, XAgingAlzheimer DiseaseDNA ReplicationHumansPhenotype

Identifiers

PMID19647374
PMCPMC2787990
OpenAlexW1996184814

What OpenQuestion holds

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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.