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Glial alterations in human prion diseases: A correlative study of astroglia, reactive microglia, protein deposition, and neuropathological lesions
Monzón M, Hernández RS, Garcés M, Sarasa R, Badiola JJ.. Medicine, 2018-04-01
Topic: Brain proteins, microglia and lab models
Background Neuroinflammation has recently been proposed to be a major component of neurodegenerative diseases. The aim of this study was to determine how the interaction between microglia and astroglia, which are the primary immune cell populations in the brain, and pathological prion protein (PrPsc) could influence the development and propagation of this neurodegenerative disease. Because a relevant role for glial response in prion disease has been clearly demonstrated in our previous studies using the natural animal model, a similar approach has been taken here using the natural human model. Methods A morphological approach has been developed to analyze cerebellar samples from patients with Creutzfeldt-Jakob disease (CJD) in comparison with healthy control cases. Histopathological lesions were assessed, and PrPsc, glial fibrillary acidic protein (GFAP) and reactive microglia were immunolabelled by specific antibodies. Furthermore, co-location studies using confocal microscopy were performed to determine the possible relationships between both types of glial cells in all samples. Results The results presented in this study support the involvement of both types of glial cells in CJD. Evidence of increased astrocyte and microglia reactivity can be observed in all CJD cases, and a close relationship between the types of glia is demonstrated by co-location studies. Conclusion Proteinopathies such as Alzheimer, Parkinson, and Huntington diseases, where aberrant proteins spread throughout the brain during disease progression, may share a molecular basis and mechanisms of propagation. Therefore, studies elucidating the interaction between gliosis and prion propagation may be relevant to these other neurodegenerative diseases and may provide new targets for therapeutic intervention.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Monzón, M., Hernández, R. S., Garcés, M., Sarasa, R., & Badiola, J. J. (2018). Glial alterations in human prion diseases: A correlative study of astroglia, reactive microglia, protein deposition, and neuropathological lesions. Medicine. https://doi.org/10.1097/md.0000000000010320
Vancouver
Monzón M, Hernández RS, Garcés M, Sarasa R, Badiola JJ. Glial alterations in human prion diseases: A correlative study of astroglia, reactive microglia, protein deposition, and neuropathological lesions. Medicine. 2018. doi:10.1097/md.0000000000010320. PMID: 29642165.
BibTeX
@article{monzon2018-29642165,
author = {Monzón, M. and Hernández, R. S. and Garcés, M. and Sarasa, R. and Badiola, J. J.},
title = {{Glial alterations in human prion diseases: A correlative study of astroglia, reactive microglia, protein deposition, and neuropathological lesions}},
journal = {Medicine},
year = {2018},
doi = {10.1097/md.0000000000010320},
pmid = {29642165},
url = {https://doi.org/10.1097/md.0000000000010320}
}
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Key findings
- Because a relevant role for glial response in prion disease has been clearly demonstrated in our previous studies using the natural animal model, a similar approach has been taken here using the natural human model.
- Results The results presented in this study support the involvement of both types of glial cells in CJD.
- Evidence of increased astrocyte and microglia reactivity can be observed in all CJD cases, and a close relationship between the types of glia is demonstrated by co-location studies.
Why it matters
This study found increased reactivity of astrocytes and microglia in brain tissue from people who had Creutzfeldt-Jakob disease, a prion disease, not Alzheimer's disease. It does not test any treatment or prevention for Alzheimer's, so it offers no direct implications for treating or curing the disease.
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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 (Medicine) |
| Journal's citation record | 3 / 4 | Medicine: journal h-index 285 (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 | 2 / 5 | 2018 — within 10 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 | 3 / 7 | Cited 29 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 2.9 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 2 / 6 | Cited 1.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Juan José Badiola: h-index 32 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Universidad de Zaragoza: institution h-index 510 (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 29642165) |
| Free to read | 2 / 2 | Free to read |
| Total | 36 / 100 | — |
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