Evidence map›Paper›PMID 30249283›Full record

ReviewJournal of neuroinflammation2018

Inflammation: the link between comorbidities, genetics, and Alzheimer's disease.

Estella A Newcombe, Judith Camats-Perna, Mallone L Silva, Nicholas Valmas, Tee Jong Huat, Rodrigo Medeiros

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
298citing papers in PubMed, 5 pooled it
22.0field-weighted citation impact, top 1% 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

298 citing papers in PubMed, 5 syntheses or guidelines pooled it, 542 citations in OpenAlex.

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  16. Plasma von Willebrand Factor and ADAMTS13 Interact WithJournal of the American Heart Association · 2026
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238 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

6 authors at 1 institution in 1 country.

Estella A NewcombeNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Building 79, Brisbane, 4072, QLD, Australia. e.newcombe@uq.edu.au.
Judith Camats-PernaNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Building 79, Brisbane, 4072, QLD, Australia.
Mallone L SilvaNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Building 79, Brisbane, 4072, QLD, Australia.
Nicholas ValmasQueensland Brain Institute, The University of Queensland, Brisbane, 4072, QLD, Australia.
Tee Jong HuatNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Building 79, Brisbane, 4072, QLD, Australia.
Rodrigo MedeirosNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Building 79, Brisbane, 4072, QLD, Australia. rodrigo.medeiros@neurula.org.ORCID http://orcid.org/0000-0002-9399-7852
The University of Queensland · AU

Funding

National Health and Medical Research Council GNT1128436National Health and Medical Research Council GNT1129192National Health and Medical Research Council GNT1139469
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, most cases of which lack a clear causative event. This has made the disease difficult to characterize and, thus, diagnose. Although some cases are genetically linked, there are many diseases and lifestyle factors that can lead to an increased risk of developing AD, including traumatic brain injury, diabetes, hypertension, obesity, and other metabolic syndromes, in addition to aging. Identifying common factors and trends between these conditions could enhance our understanding of AD and lead to the development of more effective treatments. Although the immune system is one of the body's key defense mechanisms, chronic inflammation has been increasingly linked with several age-related diseases. Moreover, it is now well accepted that chronic inflammation has an important role in the onset and progression of AD. In this review, the different inflammatory signals associated with AD and its risk factors will be outlined to demonstrate how chronic inflammation may be influencing individual susceptibility to AD. Our goal is to bring attention to potential shared signals presented by the immune system during different conditions that could lead to the development of successful treatments.

Indexed as

Alzheimer DiseaseInflammationAgingAstrocytesBrainHumansNeuronsAgingAlzheimer’s diseaseAPOE4CD33DiabetesMicrogliaNeuroinflammationObesityTBITREM2

Identifiers

PMID30249283
PMCPMC6154824
OpenAlexW2891379852

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.