Evidence map›Paper›PMID 27142644›Full record

ArticleJournal of neuropathology and experimental neurology2016

Unbiased Stereological Analysis of Reactive Astrogliosis to Estimate Age-Associated Cerebral White Matter Injury.

David W McNeal, Dieter D Brandner, Xi Gong, Nadia O Postupna, Thomas J Montine, C Dirk Keene, Stephen A Back

Abstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Brain arteriolosclerosis.Acta neuropathologica · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Transient Hypoxemia Chronically Disrupts Maturation of Preterm Fetal Ovine Subplate Neuron Arborization and Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
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

7 authors.

David W McNealFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK). backs@ohsu.edu.
Dieter D BrandnerFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).
Xi GongFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).
Nadia O PostupnaFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).
Thomas J MontineFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).
C Dirk KeeneFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).
Stephen A BackFrom the Department of Pediatrics, Oregon Health & Science University, Portland, Oregon (DWM, DDB, XG, SAB); Department of Neurology, Oregon Health & Science University, Portland, Oregon (SAB); and Department of Pathology, University of Washington, Seattle, Washington, District of Columbia (NOP, TJM, CDK).

Funding

THERAPEUTIC EFFECTS OF INTRA-NASAL INSULIN DETEMIRP50AG005136 · NIA · UNIVERSITY OF WASHINGTON · PI GRABOWSKI, THOMAS J. · 1985 to 2019
$57.2M
Furthering scientific understanding of mechanisms underlying resilience to the effects of AD pathology by incorporating state of the art quantification of gliosis, inflammation, & synaptic toxicityU01AG006781 · NIA · UNIVERSITY OF WASHINGTON · PI CRANE, PAUL K, LARSON, ERIC B · 1986 to 2020
$39.3M
White Matter Damage in Age-Related Cognitive DeclineR01AG031892 · NIA · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2016
$6.1M
Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Cellular Mechanisms of Fetal White Matter InjuryR01NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2003 to 2019
$3.7M
Protection from Stroke by SF/HGF-like Small MoleculeR43NS045373 · NINDS · ANGION BIOMEDICA CORPORATION · PI NARAYAN, PRAKASH · 2004 to 2004
$211k
NIA NIH HHS P50 AG005136NIA NIH HHS R01 AG031892NIA NIH HHS U01 AG006781NINDS NIH HHS R01 NS045737NINDS NIH HHS R01 NS054044NINDS NIH HHS R43 NS045373
6 · The paper itself

Abstract

Cerebral white matter injury (WMI) contributes to cognitive dysfunction associated with pathological aging. Because reactive astrocyte-related factors contribute to remyelination failure after WMI, we sought accurate, cost-effective, and reproducible histopathological approaches for quantification of morphometric features of reactive astrogliosis in aged human white matter in patients with vascular brain injury (VBI). We compared 7 distinct approaches to quantify the features of glial fibrillary acidic protein (GFAP)-labeled astrocytes in the prefrontal white matter of brains from patients with VBI (n = 17, mean age 88.8 years) and controls that did not exhibit VBI (n = 11, mean age 86.6 years). Only modern stereological techniques (ie, optical fractionator and spaceballs) and virtual process thickness measurements demonstrated significant changes in astrocyte number, process length, or proximal process thickness in cases with VBI relative to controls. The widely employed methods of neuropathological scoring, antibody capture assay (histelide), area fraction fractionator, and Cavalieri point counting failed to detect significant differences in GFAP expression between the groups. Unbiased stereological approaches and virtual thickness measurements provided the only sensitive and accurate means to quantify astrocyte reactivity as a surrogate marker of WMI in human brains with VBI.

Indexed as

Stereotaxic TechniquesAgedAged, 80 and overAgingAnimalsCerebrovascular TraumaCross-Sectional StudiesFemaleGlial Fibrillary Acidic ProteinGliosisHumansLeukoencephalopathiesMalePopulation SurveillanceWhite MatterGlial Fibrillary Acidic ProteinDementiaGlial fibrillary acidic proteinReactive astrogliosisStereologyVascular brain injuryWhite matter injury.

Identifiers

PMID27142644
PMCPMC6250206

What OpenQuestion holds

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Registered trials

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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.