Evidence map›Paper›PMID 33958667›Full record

ArticleScientific reports2021

nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse.

Chiara D'Angelo, Erica Costantini, Nieves Salvador, Michele Marchioni, Marta Di Nicola, Nigel H Greig, Marcella Reale

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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  9. Nicotine Activating αMolecular neurobiology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Chiara D'AngeloDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy.
Erica CostantiniDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy.
Nieves SalvadorDepartment of Molecular, Cellular and Developmental Neurobiology, Instituto Cajal-CSIC, Madrid, Spain.
Michele MarchioniDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy.
Marta Di NicolaDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy.
Nigel H GreigDrug Design and Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Marcella RealeDepartment of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy. mreale@unich.it.
University of Chieti-Pescara · ITInstituto Cajal · ESNational Institutes of Health · US

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
ALZHEIMERS RESEARCH PROJECT: Alzheimer's disease drug developmentZIAAG000469 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2019 to 2025
$6.7M
6 · The paper itself

Abstract

An evaluation of the APPswe/PS1dE9 transgenic AD mouse, presenting with the toxic Aβ1-42 deposition found in human AD, allowed us to characterize time-dependent changes in inflammatory and cholinergic markers present in AD. Astrogliosis was observed in cortex and hippocampus, with cellular loss occurring in the same areas in which Aβ plaques were present. In this setting, we found early significantly elevated levels of IL-1β and TNFα gene expression; with the hippocampus showing the highest IL-1β expression. To investigate the cholinergic anti-inflammatory pathway, the expression of nicotinic receptors (nAChRs) and cholinesterase enzymes also was evaluated. The anti-inflammatory nAChRα7, α4, and β2 were particularly increased at 6 months of age in the hippocampus, potentially as a strategy to counteract Aβ deposition and the ensuing inflammatory state. A time-dependent subunit switch to the α3β4 type occurred. Whether α3, β4 subunits have a pro-inflammatory or an inhibitory effect on ACh stimulation remains speculative. Aβ1-42 deposition, neuronal loss and increased astrocytes were detected, and a time-dependent change in components of the cholinergic anti-inflammatory pathway were observed. A greater understanding of time-dependent Aβ/nAChRs interactions may aid in defining new therapeutic strategies and novel molecular targets.

Indexed as

AcetylcholinesteraseAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAstrocytesButyrylcholinesteraseCerebral CortexCytokinesEncephalitisGene Expression ProfilingHippocampusMiceMice, TransgenicNeuronsReceptors, NicotinicAcetylcholinesteraseAmyloid beta-Protein PrecursorButyrylcholinesteraseCytokinesReceptors, Nicotinic

Identifiers

PMID33958667
PMCPMC8102527
OpenAlexW3159839169

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.