Evidence map›Paper›PMID 37048085›Full record

ReviewCells2023

Microglia Mediated Neuroinflammation in Parkinson's Disease.

Sevim Isik, Bercem Yeman Kiyak, Rumeysa Akbayir, Rama Seyhali, Tahire Arpaci

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 4 pooled it
35.9field-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

216 citing papers in PubMed, 4 syntheses or guidelines pooled it, 292 citations in OpenAlex.

  1. Pooled it
  2. Physical exercise and inflammation in Parkinson's disease: a review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Pooled it
  3. UsingInternational journal of molecular sciences · 2025
    Pooled it
  4. Pooled it
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  17. Integration of TSPO PET and fluid biomarkers to assess neuroinflammation in Parkinson's disease.European journal of nuclear medicine and molecular imaging · 2026
    Article
  18. Review
  19. Article
  20. Article

156 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

5 authors at 1 institution in 1 country.

Sevim IsikDepartment of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Uskudar University, Uskudar, Istanbul 34662, Turkey.ORCID 0000-0001-7687-6082
Bercem Yeman KiyakStem Cell Research and Application Center (USKOKMER), Uskudar University, Uskudar, Istanbul 34662, Turkey.ORCID 0000-0001-9667-3506
Rumeysa AkbayirStem Cell Research and Application Center (USKOKMER), Uskudar University, Uskudar, Istanbul 34662, Turkey.ORCID 0000-0002-3928-4966
Rama SeyhaliStem Cell Research and Application Center (USKOKMER), Uskudar University, Uskudar, Istanbul 34662, Turkey.ORCID 0000-0002-0905-1598
Tahire ArpaciStem Cell Research and Application Center (USKOKMER), Uskudar University, Uskudar, Istanbul 34662, Turkey.ORCID 0000-0001-7852-5307
Üsküdar University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's Disease (PD) is the second most common neurodegenerative disorder seen, especially in the elderly. Tremor, shaking, movement problems, and difficulty with balance and coordination are among the hallmarks, and dopaminergic neuronal loss in substantia nigra pars compacta of the brain and aggregation of intracellular protein α-synuclein are the pathological characterizations. Neuroinflammation has emerged as an involving mechanism at the initiation and development of PD. It is a complex network of interactions comprising immune and non-immune cells in addition to mediators of the immune response. Microglia, the resident macrophages in the CNS, take on the leading role in regulating neuroinflammation and maintaining homeostasis. Under normal physiological conditions, they exist as "homeostatic" but upon pathological stimuli, they switch to the "reactive state". Pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes are used to classify microglial activity with each phenotype having its own markers and released mediators. When M1 microglia are persistent, they will contribute to various inflammatory diseases, including neurodegenerative diseases, such as PD. In this review, we focus on the role of microglia mediated neuroinflammation in PD and also signaling pathways, receptors, and mediators involved in the process, presenting the studies that associate microglia-mediated inflammation with PD. A better understanding of this complex network and interactions is important in seeking new therapies for PD and possibly other neurodegenerative diseases.

Indexed as

Neurodegenerative DiseasesParkinson DiseaseHumansInflammationMicrogliaNeuroinflammatory Diseasesanti-inflammatory phenotypeM1 phenotypeM2 phenotypemicroglial activationneuroinflammationParkinson’s Diseaseα-synuclein

Identifiers

PMID37048085
PMCPMC10093562
OpenAlexW4361010653

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.