Evidence map›Paper›PMID 36593462›Full record

ArticleJournal of neuroinflammation2023

Intracellular deposits of amyloid-beta influence the ability of human iPSC-derived astrocytes to support neuronal function.

Evangelos Konstantinidis, Benjamin Portal, Tobias Mothes, Chiara Beretta, Maria Lindskog, Anna Erlandsson

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 42 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

6 authors at 1 institution in 1 country.

Evangelos KonstantinidisDepartment of Public Health and Caring Sciences, Molecular Geriatrics, Uppsala University, 751 85, Uppsala, Sweden.
Benjamin PortalDepartment of Medical Cell Biology, Uppsala University, 751 23, Uppsala, Sweden.
Tobias MothesDepartment of Public Health and Caring Sciences, Molecular Geriatrics, Uppsala University, 751 85, Uppsala, Sweden.
Chiara BerettaDepartment of Public Health and Caring Sciences, Molecular Geriatrics, Uppsala University, 751 85, Uppsala, Sweden.
Maria LindskogDepartment of Medical Cell Biology, Uppsala University, 751 23, Uppsala, Sweden.
Anna ErlandssonDepartment of Public Health and Caring Sciences, Molecular Geriatrics, Uppsala University, 751 85, Uppsala, Sweden. anna.erlandsson@pubcare.uu.se.
Uppsala University · SE

Funding

Åhlén-stiftelsen 213021Alzheimerfonden AF-968209Bertil and Ebon Norlin stiftelse 2021Gun och Bertil Stohnes Stiftelse 2021Hjärnfonden FO2021-0174O. E. och Edla Johanssons Vetenskapliga Stiftelse 2021Stiftelsen Olle Engkvist Byggmästare 215-0399Vetenskapsrådet 2021-02563
6 · The paper itself

Abstract

backgroundAstrocytes are crucial for maintaining brain homeostasis and synaptic function, but are also tightly connected to the pathogenesis of Alzheimer's disease (AD). Our previous data demonstrate that astrocytes ingest large amounts of aggregated amyloid-beta (Aβ), but then store, rather than degrade the ingested material, which leads to severe cellular stress. However, the involvement of pathological astrocytes in AD-related synaptic dysfunction remains to be elucidated.

methodsIn this study, we aimed to investigate how intracellular deposits of Aβ in astrocytes affect their interplay with neurons, focusing on neuronal function and viability. For this purpose, human induced pluripotent stem cell (hiPSC)-derived astrocytes were exposed to sonicated Αβ

resultsElectrophysiological recordings revealed significantly decreased frequency of excitatory post-synaptic currents in neurons co-cultured with Aβ-exposed astrocytes, while conditioned media from Aβ-exposed astrocytes had the opposite effect and resulted in hyperactivation of the synapses. Clearly, factors secreted from control, but not from Aβ-exposed astrocytes, benefited the wellbeing of neuronal cultures. Moreover, reactive astrocytes with Aβ deposits led to an elevated clearance of dead cells in the co-cultures.

conclusionsTaken together, our results demonstrate that inclusions of aggregated Aβ affect the reactive state of the astrocytes, as well as their ability to support neuronal function.

Indexed as

Alzheimer DiseaseInduced Pluripotent Stem CellsAmyloid beta-PeptidesAstrocytesCells, CulturedCulture Media, ConditionedHumansNeuronsAmyloid beta-PeptidesCulture Media, ConditionedAlzheimer’s diseaseAmyloid-betaAstrocytesElectrophysiologyEPSCsiPSCsNeurons

Identifiers

PMID36593462
PMCPMC9809017
OpenAlexW4313488655

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.