Evidence map›Paper›PMID 19946466›Full record

ArticleAging2009

Evidence for the progression through S-phase in the ectopic cell cycle re-entry of neurons in Alzheimer disease.

David J Bonda, Teresa A Evans, Corrado Santocanale, Jesús Catalá Llosá, Jose Viña, Vladan P Bajic, Rudy J Castellani, Sandra L Siedlak, George Perry, Mark A Smith and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

55 citing papers in PubMed, 78 citations in OpenAlex.

  1. Frontiers in pharmacology · 2026
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  16. Positive Controls in Adults and Children Support That Very Few, If Any, New Neurons Are Born in the Adult Human Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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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

11 authors at 4 institutions in 2 countries.

David J BondaDepartment of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Teresa A Evans
Corrado Santocanale
Jesús Catalá Llosá
Jose Viña
Vladan P Bajic
Rudy J Castellani
Sandra L Siedlak
George Perry
Mark A Smith
Hyoung-gon Lee
Case Western Reserve University · USOllscoil na Gaillimhe – University of Galway · IEThe University of Texas at San Antonio · USUniversity of Maryland, Baltimore · US

Funding

Role of Cell Cycle in NeurodegenerationR01AG028679 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LEE, HYOUNG-GON · 2008 to 2012
$1.6M
Neurodegeneration by reactivation of cell cycle in neuronsR21AG030096 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LEE, HYOUNG-GON · 2007 to 2008
$358k
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 AG030096NIA NIH HHS AG031364NIA NIH HHS R01 AG028679NIA NIH HHS R21 AG030096NIA NIH HHS R21 AG031364
6 · The paper itself

Abstract

Aberrant neuronal re-entry into the cell cycle is emerging as a potential pathological mechanism in Alzheimer disease (AD). However, while cyclins, cyclin dependent kinases (CDKs), and other mitotic factors are ectopically expressed in neurons, many of these proteins are also involved in other pathological and physiological processes, generating continued debate on whether such markers are truly indicative of a bona fide cell cycle process. To address this issue, here we analyzed one of the minichromosome maintenance (Mcm) proteins that plays a role in DNA replication and becomes phosphorylated by the S-phase promoting CDKs and Cdc7 during DNA synthesis. We found phosphorylated Mcm2 (pMcm2) markedly associated with neurofibrillary tangles, neuropil threads, and dystrophic neurites in AD but not in aged-matched controls. These data not only provide further evidence for cell cycle aberrations in AD, but the cytoplasmic, rather than nuclear, localization of pMcm2 suggests an abnormal cellular distribution of this important replication factor in AD that may explain resultant cell cycle stasis and consequent neuronal degeneration.

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseCell Cycle ProteinsCells, CulturedCytoplasmFemaleGene Expression RegulationHumansMaleMiddle AgedMinichromosome Maintenance Complex Component 2NeuronsNuclear ProteinsPhosphorylationCell Cycle ProteinsMCM2 protein, humanMinichromosome Maintenance Complex Component 2Nuclear ProteinsAlzheimer diseasecell cycleDNA replicationminichromosome maintenance proteinneurodegeneration

Identifiers

PMID19946466
PMCPMC2783633
OpenAlexW2333061228

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.