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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Inflammation and the immune system

Topic: Inflammation, microglia and astrocytes

Plain-language summary

Autophagy degrades phagocytosed damaged organelles, misfolded proteins, and various pathogens through lysosomes as an essential way to maintain cellular homeostasis. Autophagy is a tightly regulated cellular self-degradation process that plays a crucial role in maintaining normal cellular function and homeostasis in the body. The NLRP3 inflammasome in neuroinflammation is a vital recognition receptor in innate cellular immunity, sensing external invading pathogens and endogenous stimuli and further triggering inflammatory responses. The NLRP3 inflammasome forms an inflammatory complex by recognizing DAMPS or PAMPS, and its activation triggers caspase-1-mediated cleavage of pro-IL-1β and pro-IL-18 to promote the inflammatory response. In recent years, it has been reported that there is a complex interaction between autophagy and neuroinflammation. Strengthening autophagy can regulate the expression of NLRP3 inflammasome to reduce neuroinflammation in neurodegenerative disease and protect neurons. However, the related mechanism is not entirely clear. The formation of protein aggregates is one of the standard features of Neurodegenerative diseases. A large number of toxic protein aggregates can induce inflammation. In theory, activation of the autophagy pathway can remove the potential toxicity of protein aggregates and delay the progression of the disease. This article aims to review recent research on the interaction of autophagy, NLRP3 inflammasome, and protein aggregates in Alzheimer's disease (AD) and Parkinson's disease (PD), analyze the mechanism and provide theoretical references for further research in the future.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Lu, R., Zhang, L., & Yang, X. (2022). Interaction between autophagy and the NLRP3 inflammasome in Alzheimer's and Parkinson's disease. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2022.1018848

Vancouver

Lu R, Zhang L, Yang X. Interaction between autophagy and the NLRP3 inflammasome in Alzheimer's and Parkinson's disease. Frontiers in aging neuroscience. 2022. doi:10.3389/fnagi.2022.1018848. PMID: 36262883.

BibTeX

@article{lu2022-36262883,
  author  = {Lu, Ranran and Zhang, Lijie and Yang, Xinling},
  title   = {{Interaction between autophagy and the NLRP3 inflammasome in Alzheimer's and Parkinson's disease}},
  journal = {Frontiers in aging neuroscience},
  year    = {2022},
  doi     = {10.3389/fnagi.2022.1018848},
  pmid    = {36262883},
  url     = {https://doi.org/10.3389/fnagi.2022.1018848}
}

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How to read this study

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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

However, the related mechanism is not entirely clear.
The formation of protein aggregates is one of the standard features of Neurodegenerative diseases.
A large number of toxic protein aggregates can induce inflammation.
In theory, activation of the autophagy pathway can remove the potential toxicity of protein aggregates and delay the progression of the disease.
This article aims to review recent research on the interaction of autophagy, NLRP3 inflammasome, and protein aggregates in Alzheimer's disease (AD) and Parkinson's disease (PD), analyze the mechanism and provide theoretical references for further research in the future.

Study details

Evidence strengthLow

How this study scored 41/100

Published in a peer-reviewed 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, multicenter collaboration and free to read, so those were left out: it earned 23 of the 56 points we could judge it on, which is 41 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience)
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	3 / 5	2022 — within 6 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)
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 36262883)
Free to read	— / 2	Access not recorded — left out of this score
Points	23 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100.
Total	41 / 100	—

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