Evidence map›Paper›PMID 37055801›Full record

ArticleBehavioral and brain functions : BBF2023

Inhibition of NLRP1 inflammasome improves autophagy dysfunction and Aβ disposition in APP/PS1 mice.

Xuewang Li, Han Zhang, Liu Yang, Xianan Dong, Yuli Han, Yong Su, Weiping Li, Weizu Li

Open access · goldAbstract read
In one paragraph

Article in Behavioral and brain functions : BBF, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xuewang Li *Department of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China.
Han Zhang *Department of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China.
Liu Yang *Department of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China.
Xianan DongDepartment of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China.
Yuli HanDepartment of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China.
Yong SuDepartment of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, Anhui, China.
Weiping LiDepartment of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China. lwp19@126.com.
Weizu LiDepartment of Pharmacology, Basic Medicine College, Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei, 230032, China. liweizu@126.com.
Anhui Medical University · CN

Funding

the Major projects of Anhui Provincial Department of EducationKJ2020ZD14 KJ2020ZD14the National Natural Science Foundation of China 81671384the National Natural Science Foundation of China 81970630
6 · The paper itself

Abstract

Increasing evidence has shown that the NOD-like receptor protein 1 (NLRP1) inflammasome is associated with Aβ generation and deposition, which contributes to neuronal damage and neuronal-inflammation in Alzheimer's disease (AD). However, the specific mechanism of NLRP1 inflammasome in the pathogenesis of AD is still unclear. It has been reported that autophagy dysfunction can aggravate the pathological symptoms of AD and plays an important role in regulating Aβ generation and clearance. We hypothesized that NLRP1 inflammasome activation may induce autophagy dysfunction contributing to the progression of AD. In the present study, we observed the relationship between Aβ generation and NLRP1 inflammasome activation, as well as AMPK/mTOR mediated-autophagy dysfunction in WT 9-month-old (M) mice, APP/PS1 6 M and APP/PS1 9 M mice. Additionally, we further studied the effect of NLRP1 knockdown on cognitive function, Aβ generation, neuroinflammation and AMPK/mTOR mediated autophagy in APP/PS1 9 M mice. Our results indicated that NLRP1 inflammasome activation and AMPK/mTOR mediated-autophagy dysfunction are closely implicated in Aβ generation and deposition in APP/PS1 9 M mice, but not in APP/PS1 6 M mice. Meanwhile, we found that knockdown of NLRP1 significantly improved learning and memory impairments, decreased the expressions of NLRP1, ASC, caspase-1, p-NF-κB, IL-1β, APP, CTF-β, BACE1 and Aβ

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAMP-Activated Protein KinasesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesAutophagyDisease Models, AnimalInflammasomesMiceMice, TransgenicNLR ProteinsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesInflammasomesNLR ProteinsTOR Serine-Threonine KinasesAlzheimer's diseaseAMPK/mTORAPP/PS1 miceAutophagyNLRP1 inflammasome

Identifiers

PMID37055801
PMCPMC10100229
OpenAlexW4365453829

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.