Glial degeneration and reactive gliosis in alpha-synucleinopathies: the emerging concept of primary gliodegeneration
Croisier E, Graeber MB.. Acta neuropathologica, 2006-08-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
The concept of gliodegenerative diseases has not been widely established although there is accumulating evidence that glial cells may represent a primary target of degenerative disease processes. In the central nervous system (CNS), examples that provide a "proof of concept" include at least one alpha-synucleinopathy, multiple system atrophy (MSA), but this disease is conventionally discussed under the heading of "neurodegeneration". Additional evidence in support of primary glial affection has been reported in neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease and transmissible spongiform encephalopathies. Based on biochemical, genetic and transcriptomic studies it is also becoming increasingly clear that the molecular changes measured in whole tissue extracts, e.g. obtained from Parkinson's disease brain, are not based on a purely neuronal contribution. This important evidence has been missed in cell culture or laser capture work focusing on the neuronal cell population. Studies of animal and in vitro models of disease pathogenesis additionally suggest glial accountability for some CNS degenerative processes. This review provides a critical analysis of the evidence available to date in support of the concept of gliodegeneration, which we propose to represent an essential although largely disregarded component of the spectrum of classical "neurodegeneration". Examples from the spectrum of alpha-synucleinopathies are presented.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Croisier, E., & Graeber, M. B. (2006). Glial degeneration and reactive gliosis in alpha-synucleinopathies: the emerging concept of primary gliodegeneration. Acta neuropathologica. https://doi.org/10.1007/s00401-006-0119-z
Vancouver
Croisier E, Graeber MB. Glial degeneration and reactive gliosis in alpha-synucleinopathies: the emerging concept of primary gliodegeneration. Acta neuropathologica. 2006. doi:10.1007/s00401-006-0119-z. PMID: 16896905.
BibTeX
@article{croisier2006-16896905,
author = {Croisier, E. and Graeber, M. B.},
title = {{Glial degeneration and reactive gliosis in alpha-synucleinopathies: the emerging concept of primary gliodegeneration}},
journal = {Acta neuropathologica},
year = {2006},
doi = {10.1007/s00401-006-0119-z},
pmid = {16896905},
url = {https://doi.org/10.1007/s00401-006-0119-z}
}
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Key findings
- Based on biochemical, genetic and transcriptomic studies it is also becoming increasingly clear that the molecular changes measured in whole tissue extracts, e.g. obtained from Parkinson's disease brain, are not based on a purely neuronal contribution.
- This important evidence has been missed in cell culture or laser capture work focusing on the neuronal cell population.
- Studies of animal and in vitro models of disease pathogenesis additionally suggest glial accountability for some CNS degenerative processes.
- This review provides a critical analysis of the evidence available to date in support of the concept of gliodegeneration, which we propose to represent an essential although largely disregarded component of the spectrum of classical "neurodegeneration".
- Examples from the spectrum of alpha-synucleinopathies are presented.
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Study details
- Evidence strengthLow
How this study scored 40/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2006 — older than 20 years, still counted |
| 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16896905) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
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