Evidence map›Paper›PMID 31111399›Full record

ReviewMolecular neurobiology2019

The Role of Neuronal NLRP1 Inflammasome in Alzheimer's Disease: Bringing Neurons into the Neuroinflammation Game.

Jeremy Kean Yi Yap, Benjamin Simon Pickard, Elaine Wan Ling Chan, Sook Yee Gan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  14. Potential Role of Inflammasomes in Aging.International journal of molecular sciences · 2025
    Review
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17 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Jeremy Kean Yi YapSchool of Postgraduate Studies, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Benjamin Simon PickardStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Hamnett Wing, 161, Cathedral Street, Glasgow, G4 0RE, UK.
Elaine Wan Ling ChanInstitute for Research, Development and Innovation, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Sook Yee GanDepartment of Life Sciences, School of Pharmacy, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia. sookyee_gan@imu.edu.my.ORCID http://orcid.org/0000-0002-4826-9143
IMU University · MYUniversity of Strathclyde · GB

Funding

Ministry of Higher Education, Malaysia FRGS/1/2016/SKK08/IMU/03/1
6 · The paper itself

Abstract

The innate immune system and inflammatory response in the brain have critical impacts on the pathogenesis of many neurodegenerative diseases including Alzheimer's disease (AD). In the central nervous system (CNS), the innate immune response is primarily mediated by microglia. However, non-glial cells such as neurons could also partake in inflammatory response independently through inflammasome signalling. The NLR family pyrin domain-containing 1 (NLRP1) inflammasome in the CNS is primarily expressed by pyramidal neurons and oligodendrocytes. NLRP1 is activated in response to amyloid-β (Aβ) aggregates, and its activation subsequently cleaves caspase-1 into its active subunits. The activated caspase-1 proteolytically processes interleukin-1β (IL-1β) and interleukin-18 (IL-18) into maturation whilst co-ordinately triggers caspase-6 which is responsible for apoptosis and axonal degeneration. In addition, caspase-1 activation induces pyroptosis, an inflammatory form of programmed cell death. Studies in murine AD models indicate that the Nlrp1 inflammasome is indeed upregulated in AD and neuronal death is observed leading to cognitive decline. However, the mechanism of NLRP1 inflammasome activation in AD is particularly elusive, given its structural and functional complexities. In this review, we examine the implications of the human NLRP1 inflammasome and its signalling pathways in driving neuroinflammation in AD.

Indexed as

Adaptor Proteins, Signal TransducingAlzheimer DiseaseAnimalsBrainHumansInflammasomesInflammationNeuronsAdaptor Proteins, Signal TransducingInflammasomesAlzheimer’s diseaseCaspase-1Interleukin-18Interleukin-1βNeuroinflammationNLRP1 inflammasome

Identifiers

PMID31111399
OpenAlexW2945481468

What OpenQuestion holds

Textmetadata
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.