Evidence map›Paper›PMID 30231670›Full record

ReviewCell cycle (Georgetown, Tex.)2018

Critical role of mitosis in spontaneous late-onset Alzheimer's disease; from a Shugoshin 1 cohesinopathy mouse model.

Chinthalapally V Rao, Mudassir Farooqui, Adam S Asch, Hiroshi Y Yamada

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

Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Chinthalapally V Raoa Center for Cancer Prevention and Drug Development, Department of Medicine, Hematology/Oncology Section , University of Oklahoma Health Sciences Center (OUHSC) , Oklahoma City , OK , USA.
Mudassir Farooquia Center for Cancer Prevention and Drug Development, Department of Medicine, Hematology/Oncology Section , University of Oklahoma Health Sciences Center (OUHSC) , Oklahoma City , OK , USA.
Adam S Aschb Stephenson Cancer Center, Department of Medicine, Hematology/Oncology Section , University of Oklahoma Health Sciences Center (OUHSC) , Oklahoma City , OK , USA.
Hiroshi Y Yamadaa Center for Cancer Prevention and Drug Development, Department of Medicine, Hematology/Oncology Section , University of Oklahoma Health Sciences Center (OUHSC) , Oklahoma City , OK , USA.ORCID 0000-0002-0536-5581
University of Oklahoma Health Sciences Center · US

Funding

HMG-CoA Reductase and Polyamine Inhibitors for Prevention of Colorectal CancerR01CA094962 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI RAO, CHINTHALAPALLY V. · 2002 to 2014
$3.4M
Safer Approaches to CRC ChemopreventionR01CA213987 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI RAO, CHINTHALAPALLY V. · 2017 to 2021
$2.4M
NCI NIH HHS R01 CA094962NCI NIH HHS R01 CA213987
6 · The paper itself

Abstract

From early-onset Alzheimer's disease (EOAD) studies, the amyloid-beta hypothesis emerged as the foremost theory of the pathological causes of AD. However, how amyloid-beta accumulation is triggered and progresses toward senile plaques in spontaneous late-onset Alzheimer's disease (LOAD) in humans remains unanswered. Various LOAD facilitators have been proposed, and LOAD is currently considered a complex disease with multiple causes. Mice do not normally develop LOAD. Possibly due to the multiple causes, proposed LOAD facilitators have not been able to replicate spontaneous LOAD in mice, representing a disease modeling issue. Recently, we reported spontaneous late-onset development of amyloid-beta accumulation in brains of Shugoshin 1 (Sgo1) haploinsufficient mice, a cohesinopathy-mediated chromosome instability model. The result for the first time expands disease relevance of mitosis studies to a major disease other than cancers. Reverse-engineering of the model would shed light on the process of late-onset amyloid-beta accumulation in the brain and spontaneous LOAD development, and contribute to development of interventions for LOAD. This review will discuss the Sgo1 model, our current "three-hit hypothesis" regarding LOAD development with an emphasis on critical role of prolonged mitosis in amyloid-beta accumulation, and implications for human LOAD intervention and treatment. Abbreviations: Alzheimer's disease (AD); Late-onset Alzheimer's disease (LOAD); Early-onset Alzheimer's disease (EOAD); Shugoshin-1 (Sgo1); Chromosome Instability (CIN); apolipoprotein (Apoe); Central nervous system (CNS); Amyloid precursor protein (APP); N-methyl-d-aspartate (NMDA); Hazard ratio (HR); Cyclin-dependent kinase (CDK); Chronic Atrial Intestinal Dysrhythmia (CAID); beta-secretase 1 (BACE); phosphor-Histone H3 (p-H3); Research and development (R&D); Non-steroidal anti-inflammatory drugs (NSAIDs); Brain blood barrier (BBB).

Indexed as

MitosisAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell Cycle ProteinsChromosomal InstabilityDisease Models, AnimalHaploinsufficiencyMiceAmyloid beta-PeptidesCell Cycle Proteinsshugoshin protein, mouseAlzheimer’s disease (AD)amyloid-betabrainchromosome instability (CIN)cohesinopathymitosismouseShugoshin 1 (Sgo1)

Identifiers

PMID30231670
PMCPMC6237434
OpenAlexW2891382651

What OpenQuestion holds

Textmetadata
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.