Evidence map›Paper›PMID 33392919›Full record

ArticleCellular and molecular neurobiology2022

Expression of NLRP3 Inflammasomes in Neurogenic Niche Contributes to the Effect of Spatial Learning in Physiological Conditions but Not in Alzheimer's Type Neurodegeneration.

Yulia K Komleva, O L Lopatina, Ya V Gorina, A I Chernykh, L V Trufanova, E F Vais, E V Kharitonova, E L Zhukov, L Yu Vahtina, N N Medvedeva and 1 more

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In one paragraph

Article in Cellular and molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Yulia K KomlevaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia. yuliakomleva@mail.ru.ORCID http://orcid.org/0000-0001-5742-8356
O L LopatinaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
Ya V GorinaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
A I ChernykhResearch Institute of Molecular Medicine and Pathobiochemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
L V TrufanovaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
E F VaisThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
E V KharitonovaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
E L ZhukovDepartment of Pathological Anatomy Named After Prof. P.G. Podzolkov, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
L Yu VahtinaDepartment of Human Anatomy, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
N N MedvedevaDepartment of Human Anatomy, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
A B SalminaThe Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Ministry of Health of the Russian Federation, Professor V. F. Voino-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk, Russia.
Krasnoyarsk State Medical University · RU

Funding

Council on grants of the President of the Russian Federation 2547.2020.7Council on grants of the President of the Russian Federation 6240.2018.7
6 · The paper itself

Abstract

A common feature of neurodegenerative disorders, in particular Alzheimer's disease (AD), is a chronic neuroinflammation associated with aberrant neuroplasticity. Development of neuroinflammation affects efficacy of stem and progenitor cells proliferation, differentiation, migration, and integration of newborn cells into neural circuitry. However, precise mechanisms of neurogenesis alterations in neuroinflammation are not clear yet. It is well established that expression of NLRP3 inflammasomes in glial cells marks neuroinflammatory events, but less is known about contribution of NLRP3 to deregulation of neurogenesis within neurogenic niches and whether neural stem cells (NSCs), neural progenitor cells (NPCs) or immature neuroblasts may express inflammasomes in (patho)physiological conditions. Thus, we studied alterations of neurogenesis in rats with the AD model (intra-hippocampal injection of Aβ1-42). We found that in Aβ-affected brain, number of CD133+ cells was elevated after spatial training in the Morris water maze. The number of PSA-NCAM+ neuroblasts diminished by Aβ injection was completely restored by subsequent spatial learning. Spatial training leads to elevated expression of NLRP3 inflammasomes in the SGZ (subgranular zones): CD133+ and PSA-NCAM+ cells started to express NLRP3 in sham-operated, but not AD rats. Taken together, our data suggest that expression of NLRP3 inflammasomes in CD133+ and PSA-NCAM+ cells may contribute to stimulation of adult neurogenesis in physiological conditions, whereas Alzheimer's type neurodegeneration abolishes stimuli-induced overexpression of NLRP3 within the SGZ neurogenic niche.

Indexed as

Alzheimer DiseaseInflammasomesAnimalsNeurogenesisNLR Family, Pyrin Domain-Containing 3 ProteinRatsSpatial LearningInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratAlzheimer’s diseaseNeurogenesisNeuroinflammationNLRP3 inflammasomeSpatial learning

Identifiers

PMID33392919
PMCPMC11421703
OpenAlexW3118704517

What OpenQuestion holds

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Registered trials

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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.