Evidence map›Paper›PMID 23876085›Full record

ReviewImmunology2014

The impact of neuroimmune changes on development of amyloid pathology; relevance to Alzheimer's disease.

Marina A Lynch

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.2field-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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Neutrophil-Mediated Progression of Mild Cognitive Impairment to Dementia.International journal of molecular sciences · 2023
    Review
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  5. Investigation of the peripheral inflammation (neutrophil-lymphocyte ratio) in two neurodegenerative diseases of the central nervous system.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
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  12. The Neuro-Immune-Regulators (NIREGs) Promote Tissue Resilience; a Vital Component of the Host's Defense Strategy against Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Review
  13. Article
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  20. TLR4-activated microglia require IFN-γ to induce severe neuronal dysfunction and death in situ.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

1 author at 1 institution in 1 country.

Marina A LynchTrinity College Institute for Neuroscience, Trinity College, Dublin, Ireland.
Trinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammatory changes are a characteristic of several, if not all, neurodegenerative diseases including Alzheimer's disease and are typified by increased microglial activation. Microglia express several receptors making them highly reactive and plastic cells, and, at least in vitro, they adopt different phenotypes in a manner analogous to their peripheral counterparts, macrophages. Microglia also express numerous cell surface proteins enabling them to interact with cells and the evidence indicates that maintenance of microglia in a quiescent state relies, at least to some extent, on an interaction with neurons by means of specific ligand-receptor pairs, for example CD200-CD200R. It is clear that microglia also interact with T cells and recent evidence indicates that co-incubation of microglia with T helper type 1 cells markedly increases their activation. Under normal conditions, small numbers of activated T cells gain entry to the brain and are involved in immune surveillance but infiltration of significant numbers of T cells occurs in disease and following injury. The consequences of T cell infiltration appear to depend on the conditions, with descriptions of both neurodestructive and neuroprotective effects in animal models of different diseases. This review will discuss the modulatory effect of T cells on microglia and the impact of infiltration of T cells into the brain with a focus on Alzheimer's disease, and will propose that infiltration of interferon-γ-producing cells may be an important factor in triggering inflammation that is pathogenic and destructive.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell CommunicationDisease ProgressionHumansInterferon-gammaMicrogliaPhenotypePrognosisSignal TransductionT-LymphocytesAmyloid beta-PeptidesInterferon-gammaAlzheimer's diseaseinflammationmacrophages/monocytesneuroimmunology

Identifiers

PMID23876085
PMCPMC3930368
OpenAlexW2085961382

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.