Evidence map›Paper›PMID 27107797›Full record

ReviewProgress in neurobiology2017

Microglial phenotypes in Parkinson's disease and animal models of the disease.

Valerie Joers, Malú G Tansey, Giovanna Mulas, Anna R Carta

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 3 pooled it
15.1field-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

154 citing papers in PubMed, 3 syntheses or guidelines pooled it, 297 citations in OpenAlex.

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94 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

4 authors at 2 institutions in 2 countries.

Valerie JoersDepartment of Physiology, Emory University, Atlanta, GA, United States; Yerkes National Primate Research Center, Emory University, Atlanta, GA, United States.
Malú G TanseyDepartment of Physiology, Emory University, Atlanta, GA, United States. Electronic address: malu.tansey@emory.edu.
Giovanna MulasDepartment of Biomedical Sciences, University of Cagliari, Italy.
Anna R CartaDepartment of Biomedical Sciences, University of Cagliari, Italy. Electronic address: acarta@unica.it.
Emory University · USUniversity of Cagliari · IT

Funding

Graduate and Postdoctoral Training in ToxicologyT32ES012870 · NIEHS · EMORY UNIVERSITY · PI Carmen Joseph Marsit · 2004 to 2026
$9.1M
Role of HLA/MHCII in Parkinson's Disease PathogenesisR01NS092122 · NINDS · EMORY UNIVERSITY · PI BOSS, JEREMY M., TANSEY, MARIA DE LOURDES GAMEZ · 2015 to 2019
$1.8M
RGS10 in microglia activation and dopaminergic neuron survivalR01NS072467 · NINDS · EMORY UNIVERSITY · PI TANSEY, MARIA DE LOURDES GAMEZ · 2010 to 2014
$1.7M
NIEHS NIH HHS T32 ES012870NINDS NIH HHS R01 NS072467NINDS NIH HHS R01 NS092122
6 · The paper itself

Abstract

Over the last decade the important concept has emerged that microglia, similar to other tissue macrophages, assume different phenotypes and serve several effector functions, generating the theory that activated microglia can be organized by their pro-inflammatory or anti-inflammatory and repairing functions. Importantly, microglia exist in a heterogenous population and their phenotypes are not permanently polarized into two categories; they exist along a continuum where they acquire different profiles based on their local environment. In Parkinson's disease (PD), neuroinflammation and microglia activation are considered neuropathological hallmarks, however their precise role in relation to disease progression is not clear, yet represent a critical challenge in the search of disease-modifying strategies. This review will critically address current knowledge on the activation states of microglia as well as microglial phenotypes found in PD and in animal models of PD, focusing on the expression of surface molecules as well as pro-inflammatory and anti-inflammatory cytokine production during the disease process. While human studies have reported an elevation of both pro- or anti-inflammatory markers in the serum and CSF of PD patients, animal models have provided insights on dynamic changes of microglia phenotypes in relation to disease progression especially prior to the development of motor deficits. We also review recent evidence of malfunction at multiple steps of NFκB signaling that may have a causal interrelationship with pathological microglia activation in animal models of PD. Finally, we discuss the immune-modifying strategies that have been explored regarding mechanisms of chronic microglial activation.

Indexed as

AnimalsDisease Models, AnimalHumansMicrogliaParkinson DiseasePhenotypeImmuneMicrogliaNeurodegenerationNeuroinflammationNeuroprotectionParkinson’s

Identifiers

PMID27107797
PMCPMC5073045
OpenAlexW2343003880

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.