Evidence map›Paper›PMID 18822314›Full record

ReviewBrain research reviews2009

Toll-like receptors in neurodegeneration.

Eitan Okun, Kathleen J Griffioen, Justin D Lathia, Sung-Chun Tang, Mark P Mattson, Thiruma V Arumugam

Open access · greenAbstract readReview
In one paragraph

Review in Brain research reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed, 1 pooled it
16.4field-weighted citation impact, top 1% 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

211 citing papers in PubMed, 1 synthesis or guideline pooled it, 427 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  14. Inflammaging and Brain Aging.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Immune receptors and aging brain.Bioscience reports · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Article

151 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 2 countries.

Eitan OkunLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, 251 Bayview Boulevard, Baltimore, MD 21224, USA.
Kathleen J Griffioen
Justin D Lathia
Sung-Chun Tang
Mark P Mattson
Thiruma V Arumugam
National Institute on Aging · USNational Institutes of Health · USNational Taiwan University · TWTexas Tech University · US

Funding

Synaptic Plasticity In Aging And Neurodegenerative DisordersZIAAG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$8.5M
Neuroprotective And Neurorestorative Signaling Mechanisms in Alzheimer's DiseaseZIAAG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.7M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Apoptosis In Neurodegenerative DisordersZIAAG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Neuro-Immune Mechanisms in Brain Plasticity and AgingZIAAG000332 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$4.2M
Apoptosis In Neurodegenerative DisordersZ01AG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$2.1M
Neuroprotective &Neurorestorative Signaling MechanismsZ01AG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.9M
Cellular And Molecular Pathogenesis Of Alzheimer'sZ01AG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.9M
Synaptic Plasticity In Aging And Neurodegenerative DisordersZ01AG000317 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.7M
Intramural NIH HHS Z01 AG000312Intramural NIH HHS Z01 AG000313Intramural NIH HHS Z01 AG000314Intramural NIH HHS Z01 AG000317
6 · The paper itself

Abstract

The key roles of toll-like receptors (TLRs) as mediators of the detection and responses of immune cells to invading pathogens are well known. There are at least 13 mammalian TLRs which are integral membrane proteins with a leucine-rich extracellular domain and a cytoplasmic domain similar to that of the interleukin-1 receptor which initiates downstream signaling through kinases to activate transcription factors such as AP-1 and NFkappaB. TLRs are activated in glial cells (microglia, astrocytes and oligodendrocytes) and lymphocytes that infiltrate the nervous system in response to inflammation caused by infectious agents, tissue injury or autoimmune conditions. By inducing the production of pro-inflammatory cytokines and cell adhesion molecules in immune cells, TLRs may indirectly damage neurons in conditions such as ischemic stroke and multiple sclerosis. Recent findings suggest that neurons also express a subset of TLRs and that their activation promotes neuronal degeneration in experimental models of stroke and Alzheimer's disease. TLRs may also play roles in regulating the processes of neurogenesis and neurite outgrowth, suggesting roles in neuronal plasticity. A better understanding of the molecular and cellular biology of TLRs in the normal and diseased nervous system, may lead to novel approaches for preventing neuronal degeneration and promoting recovery of function in an array of neurodegenerative conditions.

Indexed as

AnimalsCentral Nervous SystemEncephalitisHumansImmune SystemInflammation MediatorsLymphocytesNeurodegenerative DiseasesNeurogliaSignal TransductionToll-Like ReceptorsInflammation MediatorsToll-Like Receptors

Identifiers

PMID18822314
PMCPMC2679904
OpenAlexW2144679012

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.