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Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents
Ali MU, Anwar L, Ali MH, Iqubal MK, Iqubal A, Baboota S, Ali J.. CNS & neurological disorders drug targets, 2024-01-01
Topic: Brain proteins, microglia and lab models
Alzheimer's disease (AD) is a commonly reported neurodegenerative disorder associated with dementia and cognitive impairment. The pathophysiology of AD comprises Aβ, hyperphosphorylated tau protein formation, abrupt cholinergic cascade, oxidative stress, neuronal apoptosis, and neuroinflammation. Recent findings have established the profound role of immunological dysfunction and microglial activation in the pathogenesis of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ali, M. U., Anwar, L., Ali, M. H., Iqubal, M. K., Iqubal, A., Baboota, S., et al. (2024). Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents. CNS & neurological disorders drug targets. https://doi.org/10.2174/1871527322666221223091529
Vancouver
Ali MU, Anwar L, Ali MH, Iqubal MK, Iqubal A, Baboota S, et al. Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents. CNS & neurological disorders drug targets. 2024. doi:10.2174/1871527322666221223091529. PMID: 36567300.
BibTeX
@article{ali2024-36567300,
author = {Ali, M. U. and Anwar, L. and Ali, M. H. and Iqubal, M. K. and Iqubal, A. and Baboota, S. and Ali, J.},
title = {{Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents}},
journal = {CNS \& neurological disorders drug targets},
year = {2024},
doi = {10.2174/1871527322666221223091529},
pmid = {36567300},
url = {https://doi.org/10.2174/1871527322666221223091529}
}
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
- The pathophysiology of AD comprises Aβ, hyperphosphorylated tau protein formation, abrupt cholinergic cascade, oxidative stress, neuronal apoptosis, and neuroinflammation.
- Recent findings have established the profound role of immunological dysfunction and microglial activation in the pathogenesis of AD.
- Microglial activation is a multifactorial cascade encompassing various signalling molecules and pathways such as Nrf2/NLRP3/NF-kB/p38 MAPKs/ GSK-3β.
- Additionally, deposited Aβ or tau protein triggers microglial activation and accelerates its pathogenesis.
Why it matters
This paper describes microglial activation and immunological dysfunction as having a profound role in the pathogenesis of Alzheimer's disease, involving signalling pathways such as Nrf2/NLRP3/NF-kB/p38 MAPKs/GSK-3β. It discusses the potential neuroprotective role of plant compounds, but reports no proven treatment.
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Study details
- Evidence strengthLow
How this study scored 38/100
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, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 24 of the 64 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (CNS & neurological disorders drug targets) |
| 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 | 4 / 5 | 2024 — within 3 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 (OpenAlex dates this DOI to 2022, the record says 2024; OpenAlex values not used) — 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 | 0 / 6 | No other study in this library cites it |
| 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 36567300) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 24 / 64 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 24 of the 64 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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