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Is Alzheimer's disease an inflammasomopathy?
Claudia F Pereira, Armanda E Santos, Paula I Moreira, Ana Catarina Pereira, Fabio J Sousa, Sandra M Cardoso, M Teresa Cruz. Ageing research reviews, 2019-09-29
Topic: Inflammation, microglia and astrocytes
Alzheimer's disease (AD) is the most common form of dementia in the elderly and, despite the tremendous efforts researchers have put into AD research, there are no effective options for prevention and treatment of the disease. The best way to reach this goal is to clarify the mechanisms involved in the onset and progression of AD. In the last few years the views about the drivers of AD have been changing and nowadays it is believed that neuroinflammation takes center stage in disease pathogenesis. Herein, we provide an overview about the role of neuroinflammation in AD describing the role of microglia and astroglia is this process. Then, we will debate the NLRP3 inflammasome putting the focus on its activation through the canonical, non-canonical and alternative pathways and the triggers involved herein namely endoplasmic reticulum stress, mitochondrial dysfunction, reactive oxygen species and amyloid β peptide. Data supporting the hypothesis that inflammasome-mediated peripheral inflammation may contribute to AD pathology will be presented. Finally, a brief discussion about the therapeutic potential of NLRP3 inflammasome modulation is also provided.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Pereira, C. F., Santos, A. E., Moreira, P. I., Pereira, A. C., Sousa, F. J., Cardoso, S. M., et al. (2019). Is Alzheimer's disease an inflammasomopathy? Ageing research reviews. https://doi.org/10.1016/j.arr.2019.100966
Vancouver
Pereira CF, Santos AE, Moreira PI, Pereira AC, Sousa FJ, Cardoso SM, et al. Is Alzheimer's disease an inflammasomopathy? Ageing research reviews. 2019. doi:10.1016/j.arr.2019.100966. PMID: 31577960.
BibTeX
@article{pereira2019-31577960,
author = {Pereira, Claudia F and Santos, Armanda E and Moreira, Paula I and Pereira, Ana Catarina and Sousa, Fabio J and Cardoso, Sandra M and Cruz, M Teresa},
title = {{Is Alzheimer's disease an inflammasomopathy?}},
journal = {Ageing research reviews},
year = {2019},
doi = {10.1016/j.arr.2019.100966},
pmid = {31577960},
url = {https://doi.org/10.1016/j.arr.2019.100966}
}
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
- In the last few years the views about the drivers of AD have been changing and nowadays it is believed that neuroinflammation takes center stage in disease pathogenesis.
- Herein, we provide an overview about the role of neuroinflammation in AD describing the role of microglia and astroglia is this process.
- Then, we will debate the NLRP3 inflammasome putting the focus on its activation through the canonical, non-canonical and alternative pathways and the triggers involved herein namely endoplasmic reticulum stress, mitochondrial dysfunction, reactive oxygen species and amyloid β peptide.
- Data supporting the hypothesis that inflammasome-mediated peripheral inflammation may contribute to AD pathology will be presented.
- Finally, a brief discussion about the therapeutic potential of NLRP3 inflammasome modulation is also provided.
Study details
- Evidence strengthLow
How this study scored 39/100
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. 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, multi-centre collaboration and free to read, so those were left out: it earned 22 of the 56 points we could judge it on, which is 39 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Ageing research reviews) |
| 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 | 2 / 5 | 2019 — 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 | — / 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31577960) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 22 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 22 of the 56 points we could judge it on is 39 out of 100. |
| Total | 39 / 100 | — |
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