Evidence map›Paper›PMID 28285346›Full record

ArticleNeurotoxicity research2017

Complex Changes in the Innate and Adaptive Immunity Accompany Progressive Degeneration of the Nigrostriatal Pathway Induced by Intrastriatal Injection of 6-Hydroxydopamine in the Rat.

Giulia Ambrosi, Natasa Kustrimovic, Francesca Siani, Emanuela Rasini, Silvia Cerri, Cristina Ghezzi, Giuseppe Dicorato, Sofia Caputo, Franca Marino, Marco Cosentino and 1 more

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
  10. Review
  11. Article
  12. T cells, α-synuclein and Parkinson disease.Handbook of clinical neurology · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. α-Synuclein in Parkinson's disease: causal or bystander?Journal of neural transmission (Vienna, Austria : 1996) · 2019
    Review
  19. Article
  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

11 authors at 2 institutions in 1 country.

Giulia AmbrosiLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Natasa KustrimovicCenter of Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Francesca SianiLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Emanuela RasiniCenter of Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Silvia CerriLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Cristina GhezziLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Giuseppe DicoratoLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Sofia CaputoLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy.
Franca MarinoCenter of Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Marco CosentinoCenter of Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Fabio BlandiniLaboratory of Functional Neurochemistry, Center for Research in Neurodegenerative Diseases, C. Mondino National Neurological Institute, Via Mondino, 2, 27100, Pavia, Italy. fabio.blandini@mondino.it.
Fondazione Istituto Neurologico Nazionale Casimiro Mondino · ITUniversity of Insubria · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated changes in innate and adaptive immunity paralleling the progressive nigrostriatal damage occurring in a neurotoxic model of Parkinson's disease (PD) based on unilateral infusion of 6-hydroxydopamine (6-OHDA) into the rat striatum. A time-course analysis was conducted to assess changes in morphology (activation) and cell density of microglia and astrocytes, microglia polarization (M1 vs. M2 phenotype), lymphocyte infiltration in the lesioned substantia nigra pars compacta (SNc), and modifications of CD8+ and subsets of CD4+ T cell in peripheral blood accompanying nigrostriatal degeneration. Confirming previous results, we observed slightly different profiles of activation for astrocytes and microglia paralleling nigral neuronal loss. For astrocytes, morphological changes and cell density increases were mostly evident at the latest time points (14 and 28 days post-surgery), while moderate microglia activation was present since the earliest time point. For the first time, in this model, we described the time-dependent profile of microglia polarization. Activated microglia clearly expressed the M2 phenotype in the earlier phase of the experiment, before cell death became manifest, gradually shifting to the M1 phenotype as SNc cell death started. In parallel, a reduction in the percentage of circulating CD4+ T regulatory (Treg) cells, starting as early as day 3 post-6-OHDA injection, was detected in 6-OHDA-injected rats. Our data show that nigrostriatal degeneration is associated with complex changes in central and peripheral immunity. Microglia activation and polarization, Treg cells, and the factors involved in their cross-talk should be further investigated as targets for the development of therapeutic strategies for disease modification in PD.

Indexed as

Adaptive ImmunityAnimalsAntigens, CDAstrocytesCorpus StriatumDisease Models, AnimalDisease ProgressionEncephalitisFlow CytometryGlial Fibrillary Acidic ProteinLymphocytesMaleOxidopamineParkinson DiseaseRatsRats, Sprague-DawleyAntigens, CDGlial Fibrillary Acidic ProteinOxidopamineSympatholyticsTyrosine 3-Monooxygenase6-OHDAAstrocytesMicrogliaParkinson’s diseaseRatT regulatory cells

Identifiers

PMID28285346
OpenAlexW2593337312

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.