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Dynamic changes in pro- and anti-inflammatory cytokines in microglia after PPAR-γ agonist neuroprotective treatment in the MPTPp mouse model of progressive Parkinson's disease
Pisanu A, Lecca D, Mulas G, Wardas J, Simbula G, Spiga S, Carta AR.. Neurobiology of disease, 2014-08-15
Topic: Brain proteins, microglia and lab models
Neuroinflammatory changes play a pivotal role in the progression of Parkinson's disease (PD) pathogenesis. Recent findings have suggested that activated microglia may polarize similarly to peripheral macrophages in the central nervous system (CNS), assuming a pro-inflammatory M1 phenotype or the alternative anti-inflammatory M2 phenotype via cytokine production. A skewed M1 activation over M2 has been related to disease progression in Alzheimer disease, and modulation of microglia polarization may be a therapeutic target for neuroprotection.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Pisanu, A., Lecca, D., Mulas, G., Wardas, J., Simbula, G., Spiga, S., et al. (2014). Dynamic changes in pro- and anti-inflammatory cytokines in microglia after PPAR-γ agonist neuroprotective treatment in the MPTPp mouse model of progressive Parkinson's disease. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2014.08.011
Vancouver
Pisanu A, Lecca D, Mulas G, Wardas J, Simbula G, Spiga S, et al. Dynamic changes in pro- and anti-inflammatory cytokines in microglia after PPAR-γ agonist neuroprotective treatment in the MPTPp mouse model of progressive Parkinson's disease. Neurobiology of disease. 2014. doi:10.1016/j.nbd.2014.08.011. PMID: 25134730.
BibTeX
@article{pisanu2014-25134730,
author = {Pisanu, A. and Lecca, D. and Mulas, G. and Wardas, J. and Simbula, G. and Spiga, S. and Carta, A. R.},
title = {{Dynamic changes in pro- and anti-inflammatory cytokines in microglia after PPAR-γ agonist neuroprotective treatment in the MPTPp mouse model of progressive Parkinson's disease}},
journal = {Neurobiology of disease},
year = {2014},
doi = {10.1016/j.nbd.2014.08.011},
pmid = {25134730},
url = {https://doi.org/10.1016/j.nbd.2014.08.011}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Recent findings have suggested that activated microglia may polarize similarly to peripheral macrophages in the central nervous system (CNS), assuming a pro-inflammatory M1 phenotype or the alternative anti-inflammatory M2 phenotype via cytokine production.
- A skewed M1 activation over M2 has been related to disease progression in Alzheimer disease, and modulation of microglia polarization may be a therapeutic target for neuroprotection.
- By using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-probenecid (MPTPp) mouse model of progressive PD, we investigated dynamic changes in the production of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, and anti-inflammatory cytokines, such as transforming growth factor (TGF)-β and IL-10, within Iba-1-positive cells in the substantia nigra compacta (SNc).
- In addition, to further characterize changes in the M2 phenotype, we measured CD206 in microglia.
Why it matters
This mouse study of a Parkinson's disease model discusses microglial polarization and its possible link to Alzheimer's disease progression, suggesting modulation of microglia as a possible neuroprotective target. It is an animal study and provides no treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of disease) |
| Journal's citation record | 2 / 4 | Neurobiology of Disease: journal h-index 225 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2014 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 269 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 19.2 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 4 / 6 | Cited 9.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 42 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Anna Rosa Carta: h-index 36 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | National Research Council: institution h-index 840 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25134730) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.nbd.2014.08.011
- PubMed: 25134730
- Original source →
- Free full text: DOAJ (DOAJ: Directory of Open Access Journals) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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