Evidence map›Paper›PMID 35775627›Full record

ArticleeLife2022

Synaptic location is a determinant of the detrimental effects of α-synuclein pathology to glutamatergic transmission in the basolateral amygdala.

Liqiang Chen, Chetan Nagaraja, Samuel Daniels, Zoe A Fisk, Rachel Dvorak, Lindsay Meyerdirk, Jennifer A Steiner, Martha L Escobar Galvis, Michael X Henderson, Maxime W C Rousseaux and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

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  14. Research Priorities on the Role of α-Synuclein in Parkinson's Disease Pathogenesis.Movement disorders : official journal of the Movement Disorder Society · 2024
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  19. From Synaptic Physiology to Synaptic Pathology: The Enigma of α-Synuclein.International journal of molecular sciences · 2024
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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

12 authors at 3 institutions in 3 countries.

Liqiang Chen *Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.ORCID 0000-0003-3236-1129
Chetan Nagaraja *Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.
Samuel Daniels *Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.
Zoe A FiskAligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, United States.
Rachel DvorakDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.
Lindsay MeyerdirkDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.
Jennifer A SteinerDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.ORCID 0000-0003-0953-1310
Martha L Escobar GalvisDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.ORCID 0000-0001-8400-9392
Michael X HendersonDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.
Maxime W C RousseauxAligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, United States.
Patrik BrundinPharma Research and Early Development (pRED), F. Hoffman-La Roche, Little Falls, United States.
Hong-Yuan ChuDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, United States.ORCID 0000-0003-0923-683X
Van Andel Institute · USUniversity of Ottawa · CARoche (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presynaptic protein α-synuclein (αSyn) has been suggested to be involved in the pathogenesis of Parkinson's disease (PD). In PD, the amygdala is prone to develop insoluble αSyn aggregates, and it has been suggested that circuit dysfunction involving the amygdala contributes to the psychiatric symptoms. Yet, how αSyn aggregates affect amygdala function is unknown. In this study, we examined αSyn in glutamatergic axon terminals and the impact of its aggregation on glutamatergic transmission in the basolateral amygdala (BLA). We found that αSyn is primarily present in the vesicular glutamate transporter 1-expressing (vGluT1

Indexed as

Basolateral Nuclear ComplexParkinson Diseasealpha-SynucleinAnimalsMiceNeuronsPresynaptic TerminalsSynapsesSynaptic Transmissionalpha-Synucleinalpha-synucleinamygdalamouseneuroscienceparkinson's diseasepsychiatric symptomssynapsesynucleinopathiesvGlut

Identifiers

PMID35775627
PMCPMC9286736
OpenAlexW4283741897

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.