Evidence map›Paper›PMID 25904805›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Closed head injury in an age-related Alzheimer mouse model leads to an altered neuroinflammatory response and persistent cognitive impairment.

Scott J Webster, Linda J Van Eldik, D Martin Watterson, Adam D Bachstetter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 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 3 institutions in 2 countries.

Scott J WebsterSanders-Brown Center on Aging.
Linda J Van EldikSanders-Brown Center on Aging, Department of Anatomy and Neurobiology, Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536, and.
D Martin WattersonDepartment of Pharmacology, Northwestern University, Chicago, Illinois 60611.ORCID http://orcid.org/0000-0001-7605-5866
Adam D BachstetterSanders-Brown Center on Aging, adam.bachstetter@uky.edu.
Institute on Aging · USNorthwestern University · USUniversity of Kentucky · US

Funding

Involvement of myelin integrity in Alzheimer's disease pathogenesisK99AG044445 · NIA · UNIVERSITY OF KENTUCKY · PI BACHSTETTER, ADAM D · 2014 to 2015
$175k
Dysregulated neuroinflammation: a novel target for neurodegeneration after TBIF32NS084605 · NINDS · UNIVERSITY OF KENTUCKY · PI WEBSTER, SCOTT J · 2013 to 2014
$102k
NIA NIH HHS K99 AG044445NIA NIH HHS K99AG044445NINDS NIH HHS F32 NS084605
6 · The paper itself

Abstract

Epidemiological studies have associated increased risk of Alzheimer's disease (AD)-related clinical symptoms with a medical history of head injury. Currently, little is known about pathophysiology mechanisms linked to this association. Persistent neuroinflammation is one outcome observed in patients after a single head injury. Neuroinflammation is also present early in relevant brain regions during AD pathology progression. In addition, previous mechanistic studies in animal models link neuroinflammation as a contributor to neuropathology and cognitive impairment in traumatic brain injury (TBI) or AD-related models. Therefore, we explored the potential interplay of neuroinflammatory responses in TBI and AD by analysis of the temporal neuroinflammatory changes after TBI in an AD model, the APP/PS1 knock-in (KI) mouse. Discrete temporal aspects of astrocyte, cytokine, and chemokine responses in the injured KI mice were delayed compared with the injured wild-type mice, with a peak neuroinflammatory response in the injured KI mice occurring at 7 d after injury. The neuroinflammatory responses were more persistent in the injured KI mice, leading to a chronic neuroinflammation. At late time points after injury, KI mice exhibited a significant impairment in radial arm water maze performance compared with sham KI mice or injured wild-type mice. Intervention with a small-molecule experimental therapeutic (MW151) that selectively attenuates proinflammatory cytokine production yielded improved cognitive behavior outcomes, consistent with a link between neuroinflammatory responses and altered risk for AD-associated pathology changes with head injury.

Indexed as

AgingDisease Models, AnimalAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAstrocytesBrain InjuriesChemokinesCognition DisordersCytokinesDisease ProgressionFemaleGene Knock-In TechniquesHead Injuries, ClosedInflammation MediatorsMale2-(4-(4-methyl-6-phenylpyridazin-3-yl)piperazin-1-yl)pyrimidineAmyloid beta-Protein PrecursorChemokinesCytokinesInflammation MediatorsPyridazinesPyrimidinesamyloid plaqueastrocytescytokinesmicroglianeuroinflammationtraumatic brain injury

Identifiers

PMID25904805
PMCPMC4405562
OpenAlexW2128358339

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.