Evidence map›Paper›PMID 25426068›Full record

ReviewFrontiers in aging neuroscience2014

Bioenergetic dysfunction and inflammation in Alzheimer's disease: a possible connection.

Heather M Wilkins, Steven M Carl, Alison C S Greenlief, Barry W Festoff, Russell H Swerdlow

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  16. Neuroinflammatory Responses and Parkinson' Disease: Pathogenic Mechanisms and Therapeutic Targets.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  17. Article
  18. Review
  19. Thrombin and theFrontiers in neurology · 2019
    Review
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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

5 authors at 1 institution in 1 country.

Heather M WilkinsDepartment of Neurology, University of Kansas Medical Center , Kansas City, KS , USA ; University of Kansas Alzheimer's Disease Center, University of Kansas Medical Center , Kansas City, KS , USA.
Steven M CarlUniversity of Kansas Alzheimer's Disease Center, University of Kansas Medical Center , Kansas City, KS , USA.
Alison C S GreenliefUniversity of Kansas Alzheimer's Disease Center, University of Kansas Medical Center , Kansas City, KS , USA.
Barry W FestoffDepartment of Neurology, University of Kansas Medical Center , Kansas City, KS , USA ; Department of Pharmacology, University of Kansas Medical Center , Kansas City, KS , USA ; Department of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, KS , USA ; pHLOGISTIX Neurodiagnostics , Lenexa, KS , USA.
Russell H SwerdlowDepartment of Neurology, University of Kansas Medical Center , Kansas City, KS , USA ; University of Kansas Alzheimer's Disease Center, University of Kansas Medical Center , Kansas City, KS , USA ; Department of Molecular and Integrative Physiology, University of Kansas Medical Center , Kansas City, KS , USA ; Department of Biochemistry and Molecular Biology, University of Kansas Medical Center , Kansas City, KS , USA.
University of Kansas Medical Center · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
NIA NIH HHS P30 AG035982
6 · The paper itself

Abstract

Inflammation is observed in Alzheimer's disease (AD) subject brains. Inflammation-relevant genes are increasingly implicated in AD genetic studies, and inflammatory cytokines to some extent even function as peripheral biomarkers. What underlies AD inflammation is unclear, but no "foreign" agent has been implicated. This suggests that internally produced damage-associated molecular pattern (DAMPs) molecules may drive inflammation in AD. A more complete characterization and understanding of AD-relevant DAMPs could advance our understanding of AD and suggest novel therapeutic strategies. In this review, we consider the possibility that mitochondria, intracellular organelles that resemble bacteria in many ways, trigger and maintain chronic inflammation in AD subjects. Data supporting the possible nexus between AD-associated bioenergetic dysfunction are discussed.

Indexed as

Alzheimer’s diseasebioenergeticsDAMPinflammationmitochondria

Identifiers

PMID25426068
PMCPMC4226164
OpenAlexW2062537322

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.