Evidence map›Paper›PMID 29541852›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Neuroinflammation in L-DOPA-induced dyskinesia: beyond the immune function.

Augusta Pisanu, Laura Boi, Giovanna Mulas, Saturnino Spiga, Sandro Fenu, Anna R Carta

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Article
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  9. Article
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  11. Review
  12. Review
  13. Sequestration of Inflammation in Parkinson's Disease via Stem Cell Therapy.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
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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 2 institutions in 1 country.

Augusta PisanuInstitute of Neuroscience, National Research Council, SS 554 km 4.500, Monserrato, 09042, Cagliari, Italy.
Laura BoiDepartment of Biomedical Sciences, University of Cagliari, Cittadella Universitaria di Monserrato, S.P. N. 8, Monserrato, 09042, Cagliari, Italy.
Giovanna MulasDepartment of Life and Environmental Sciences, University of Cagliari, Via Fiorelli 1, Cagliari, Italy.
Saturnino SpigaDepartment of Life and Environmental Sciences, University of Cagliari, Via Fiorelli 1, Cagliari, Italy.
Sandro FenuDepartment of Biomedical Sciences, University of Cagliari, Cittadella Universitaria di Monserrato, S.P. N. 8, Monserrato, 09042, Cagliari, Italy.
Anna R CartaDepartment of Biomedical Sciences, University of Cagliari, Cittadella Universitaria di Monserrato, S.P. N. 8, Monserrato, 09042, Cagliari, Italy. acarta@unica.it.
University of Cagliari · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is a main component of Parkinson's disease (PD) neuropathology, where unremitting reactive microglia and microglia-secreted soluble molecules such as cytokines, contribute to the neurodegenerative process as part of an aberrant immune reaction. Besides, pro-inflammatory cytokines, predominantly TNF-α, play an important neuromodulatory role in the healthy and diseased brain, being involved in neurotransmitter metabolism, synaptic scaling and brain plasticity. Recent preclinical studies have evidenced an exacerbated neuroinflammatory reaction in the striatum of parkinsonian rats that developed dyskinetic responses following L-DOPA administration. These findings prompted investigation of non-neuronal mechanisms of L-DOPA-induced dyskinesia (LID) involving glial cells and glial-secreted soluble molecules. Hence, besides the classical mechanisms of LID that include abnormal corticostriatal neurotransmission and maladaptive changes in striatal medium spiny neurons (MSNs), here we review studies supporting a role of striatal neuroinflammation in the development of LID, with a focus on microglia and the pro-inflammatory cytokine TNF-α. Moreover, we discuss several mechanisms that have been involved in the development of LID, which are directly or indirectly under the control of TNF-α, and might be abnormally affected by its chronic overproduction and release by microglia in PD. It is proposed that TNF-α may contribute to the altered neuronal responses occurring in LID by targeting receptor trafficking and function in MSNs, but also dopamine synthesis in preserved dopaminergic terminals and serotonin metabolism in serotonergic neurons. Therapeutic approaches specifically targeting glial-secreted cytokines may represent a novel target for preventing or treating LID.

Indexed as

AnimalsAntiparkinson AgentsDyskinesia, Drug-InducedHumansInflammationLevodopaTumor Necrosis Factor-alphaAntiparkinson AgentsLevodopaTumor Necrosis Factor-alphaCytokineDyskinesiaInflammationMicrogliaParkinson

Identifiers

PMID29541852
OpenAlexW2792641073

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.