Evidence map›Paper›PMID 34769018›Full record

ArticleInternational journal of molecular sciences2021

NLRP3 Inflammasome Blocking as a Potential Treatment of Central Insulin Resistance in Early-Stage Alzheimer's Disease.

Yulia K Komleva, Ilia V Potapenko, Olga L Lopatina, Yana V Gorina, Anatoly Chernykh, Elena D Khilazheva, Alla B Salmina, Anton N Shuvaev

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. 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
0.8field-weighted citation impact, top 35% 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, 20 citations in OpenAlex.

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  11. Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022
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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 2 institutions in 1 country.

Yulia K KomlevaDepartment of Biochemistry, Medical, Pharmaceutical & Toxicological Chemistry, Krasnoyarsk State Medical University Named after Prof. V.F. Voino-Yasenetsky, 660022 Krasnoyarsk, Russia.ORCID 0000-0001-5742-8356
Ilia V PotapenkoResearch Institute of Molecular Medicine and Pathobiochemistry, 660022 Krasnoyarsk, Russia.ORCID 0000-0001-9743-8700
Olga L LopatinaDepartment of Biochemistry, Medical, Pharmaceutical & Toxicological Chemistry, Krasnoyarsk State Medical University Named after Prof. V.F. Voino-Yasenetsky, 660022 Krasnoyarsk, Russia.
Yana V GorinaDepartment of Biochemistry, Medical, Pharmaceutical & Toxicological Chemistry, Krasnoyarsk State Medical University Named after Prof. V.F. Voino-Yasenetsky, 660022 Krasnoyarsk, Russia.
Anatoly ChernykhResearch Institute of Molecular Medicine and Pathobiochemistry, 660022 Krasnoyarsk, Russia.
Elena D KhilazhevaDepartment of Biochemistry, Medical, Pharmaceutical & Toxicological Chemistry, Krasnoyarsk State Medical University Named after Prof. V.F. Voino-Yasenetsky, 660022 Krasnoyarsk, Russia.
Alla B SalminaResearch Institute of Molecular Medicine and Pathobiochemistry, 660022 Krasnoyarsk, Russia.
Anton N ShuvaevResearch Institute of Molecular Medicine and Pathobiochemistry, 660022 Krasnoyarsk, Russia.
Krasnoyarsk State Medical University · RUResearch Center of Neurology · RU

Funding

Russian Federation for State support of the leading scientific schools of the Russian Federation 2547.2020.7.
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a devastating neurodegenerative disorder. In recent years, attention of researchers has increasingly been focused on studying the role of brain insulin resistance (BIR) in the AD pathogenesis. Neuroinflammation makes a significant contribution to the BIR due to the activation of NLRP3 inflammasome. This study was devoted to the understanding of the potential therapeutic roles of the NLRP3 inflammasome in neurodegeneration occurring concomitant with BIR and its contribution to the progression of emotional disorders.

methodsTo test the impact of innate immune signaling on the changes induced by Aβ1-42 injection, we analyzed animals carrying a genetic deletion of the Nlrp3 gene. Thus, we studied the role of NLRP3 inflammasomes in health and neurodegeneration in maintaining brain insulin signaling using behavioral, electrophysiological approaches, immunohistochemistry, ELISA and real-time PCR.

resultsWe revealed that NLRP3 inflammasomes are required for insulin-dependent glucose transport in the brain and memory consolidation. Conclusions NLRP3 knockout protects mice against the development of BIR: Taken together, our data reveal the protective role of Nlrp3 deletion in the regulation of fear memory and the development of Aβ-induced insulin resistance, providing a novel target for the clinical treatment of this disorder.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainInflammasomesInsulin ResistanceMaleMiceMice, Inbred C57BLMice, KnockoutNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinAmyloid beta-PeptidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseAlzheimer’s diseasebrain insulin resistancecognitive disordersneuroinflammationNLRP3 inflammasome

Identifiers

PMID34769018
PMCPMC8583950
OpenAlexW3211299334

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.