Evidence map›Paper›PMID 27531189›Full record

ReviewBrain, behavior, and immunity2017

Does B lymphocyte-mediated autoimmunity contribute to post-stroke dementia?

Kristian P Doyle, Marion S Buckwalter

Open access · greenAbstract readReview
In one paragraph

Review in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Stroke and dementia risk: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2018
    Pooled it
  2. Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026
    Review
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  17. Updates of the role of B-cells in ischemic stroke.Frontiers in cellular neuroscience · 2024
    Review
  18. Role of the gut microbiota in complications after ischemic stroke.Frontiers in cellular and infection microbiology · 2024
    Review
  19. Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Kristian P DoyleDepartment of Immunobiology, Department of Neurology, and the Arizona Center on Aging, University of Arizona, Tucson, AZ, USA. Electronic address: doylekr@email.arizona.edu.
Marion S BuckwalterDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: marion.buckwalter@stanford.edu.
Stanford University · USUniversity of Arizona · US

Funding

Inflammation and delayed cognitive dysfunction after strokeR00NR013593 · NINR · UNIVERSITY OF ARIZONA · PI DOYLE, KRISTIAN PAUL · 2014 to 2016
$686k
Delayed cognitive impairment after strokeR21NS078571 · NINDS · STANFORD UNIVERSITY · PI BUCKWALTER, MARION S · 2012 to 2013
$427k
NINDS NIH HHS R21 NS078571NINR NIH HHS R00 NR013593
6 · The paper itself

Abstract

Post-stroke cognitive decline and dementia pose a significant public health problem, with 30% of stroke survivors suffering from dementia. The reason for this high prevalence is not well understood. Pathogenic B cell responses to the damaged CNS are one possible contributing factor. B-lymphocytes and antibodies are present in and around the stroke core of some human subjects who die with stroke and dementia, and mice that develop delayed cognitive dysfunction after stroke have clusters of B-lymphocytes in the stroke lesion, and antibody infiltration in the stroked hemisphere. The ablation of B-lymphocytes prevents post-stroke cognitive impairment in mice. Multiple drugs that target B cells are FDA approved, and so if pathogenic B cell responses are occurring in a subset of stroke patients, this is potentially treatable. However, it has also been demonstrated that regulatory B cells can be beneficial in mouse models of stroke. Consequently, it is important to understand the relative contribution of B-lymphocytes to recovery versus pathogenicity, and if this balance is heterogeneous in different individuals. Therefore, the purpose of this review is to summarize the current state of knowledge with regard to the role of B-lymphocytes in the etiology of post-stroke dementia.

Indexed as

AutoimmunityAnimalsB-LymphocytesDementiaHumansStrokeAlzheimer’s DiseaseAutoantibodyAutoimmuneDementiaLymphocyteStrokeVascular dementia

Identifiers

PMID27531189
PMCPMC5305803
OpenAlexW2510727969

What OpenQuestion holds

Textmetadata
LicenceTDM
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.