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Glial cell dysregulation: a new perspective on Alzheimer disease
von Bernhardi R.. Neurotoxicity research, 2007-12-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer disease (AD) is a major cause of dementia. Several mechanisms have been postulated to explain its pathogenesis, beta-amyloid (A beta toxicity, cholinergic dysfunction, Tau hyper-phosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques, among others. Glial cells are the major producers of inflammatory mediators, and cytotoxic activation of glial cells is linked to several neurodegenerative diseases; however, whether inflammation is a consequence or the cause of neurodegeneration is still unclear.
Key findings
- Several mechanisms have been postulated to explain its pathogenesis, beta-amyloid (A beta toxicity, cholinergic dysfunction, Tau hyper-phosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques, among others.
- Glial cells are the major producers of inflammatory mediators, and cytotoxic activation of glial cells is linked to several neurodegenerative diseases; however, whether inflammation is a consequence or the cause of neurodegeneration is still unclear.
- I propose that inflammation and cellular stress associated with aging are key events in the development of AD through the induction of glial dysfunction.
- Dysregulated inflammatory response can elicit glial cell activation by compounds which are normally poorly reactive.
Why it matters
This review discusses glial cell dysregulation and inflammation in Alzheimer's disease, noting it is still unclear whether inflammation is a cause or a consequence of neurodegeneration. It does not report any treatment, cure or prevention.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurotoxicity research) |
| Journal's citation record | 1 / 4 | Neurotoxicity Research: journal h-index 103 (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 | 2007 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 138 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.6 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 3 / 6 | Cited 4.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Rommy von Bernhardi M.: h-index 41 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Pontificia Universidad Católica de Chile: institution h-index 508 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18201950) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
von Bernhardi, R. (2007). Glial cell dysregulation: a new perspective on Alzheimer disease. Neurotoxicity research. https://doi.org/10.1007/bf03033906
Vancouver
von Bernhardi R. Glial cell dysregulation: a new perspective on Alzheimer disease. Neurotoxicity research. 2007. doi:10.1007/bf03033906. PMID: 18201950.
BibTeX
@article{vonbernhardi2007-18201950,
author = {von Bernhardi, R.},
title = {{Glial cell dysregulation: a new perspective on Alzheimer disease}},
journal = {Neurotoxicity research},
year = {2007},
doi = {10.1007/bf03033906},
pmid = {18201950},
url = {https://doi.org/10.1007/bf03033906}
}
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