Evidence map›Paper›PMID 37834299›Full record

ArticleInternational journal of molecular sciences2023

Aβ1-42 Accumulation Accompanies Changed Expression of Ly6/uPAR Proteins, Dysregulation of the Cholinergic System, and Degeneration of Astrocytes in the Cerebellum of Mouse Model of Early Alzheimer Disease.

Maxim L Bychkov, Aizek B Isaev, Alexander A Andreev-Andrievskiy, Konstantin Petrov, Alexander S Paramonov, Mikhail P Kirpichnikov, Ekaterina N Lyukmanova

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 10 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

7 authors at 4 institutions in 1 country.

Maxim L BychkovShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 119997 Moscow, Russia.
Aizek B IsaevShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 119997 Moscow, Russia.ORCID 0009-0007-9913-1842
Alexander A Andreev-AndrievskiyInterdisciplinary Scientific and Educational School of Moscow University «Molecular Technologies of the Living Systems and Synthetic Biology», Faculty of Biology, Lomonosov Moscow State University, 119234 Moscow, Russia.ORCID 0000-0002-1173-8153
Konstantin PetrovArbuzov Institute of Organic and Physical Chemistry, Federal Research Center "Kazan Scientific Center of the Russian Academy of Sciences", Arbuzov Str., 8, 420088 Kazan, Russia.
Alexander S ParamonovShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 119997 Moscow, Russia.
Mikhail P KirpichnikovShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 119997 Moscow, Russia.
Ekaterina N LyukmanovaShemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 119997 Moscow, Russia.
Institute of Bioorganic Chemistry · RULomonosov Moscow State University · RUMoscow Institute of Physics and Technology · RUA.E. Arbuzov Institute of Organic and Physical Chemistry · RU

Funding

Ministry of Science and Higher Education of the Russian Federation 075-15-2021-1067Russian Science Foundation 19-74-20176
6 · The paper itself

Abstract

Alzheimer disease (AD) is a widespread neurodegenerative disease characterized by the accumulation of oligomeric toxic forms of β-amyloid (Aβ1-42) and dysfunction of the cholinergic system in the different brain regions. However, the exact mechanisms of AD pathogenesis and the role of the nicotinic acetylcholine receptors (nAChRs) in the disease progression remain unclear. Here, we revealed a decreased expression of a number of the Ly6/uPAR proteins targeting nAChRs in the cerebellum of 2xTg-AD mice (model of early AD) in comparison with non-transgenic mice both at mRNA and protein levels. We showed that co-localization of one of them, - neuromodulator Lynx1, with α7-nAChR was diminished in the vicinity of cerebellar astrocytes of 2xTg-AD mice, while Aβ1-42 co-localization with this receptor present was increased. Moreover, the expression of anti-inflammatory transcription factor KLF4 regulating transcription of the

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesReceptors, Nicotinicalpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-PeptidesAnimalsAstrocytesCerebellumCholinergic AgentsMicePeptide Fragmentsalpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-Peptidesamyloid beta-protein (1-42)Cholinergic AgentsPeptide FragmentsReceptors, NicotinicAlzheimer diseaseastrocytesLy6/uPARLynx1Lypd6motor memorynicotinic acetylcholine receptorPSCASLURP-1

Identifiers

PMID37834299
PMCPMC10573428
OpenAlexW4387310127

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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.