Evidence map›Paper›PMID 36827984›Full record

ArticleNeuron2023

EndophilinA-dependent coupling between activity-induced calcium influx and synaptic autophagy is disrupted by a Parkinson-risk mutation.

Adekunle T Bademosi, Marianna Decet, Sabine Kuenen, Carles Calatayud, Jef Swerts, Sandra F Gallego, Nils Schoovaerts, Spyridoula Karamanou, Nikolaos Louros, Ella Martin and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Neuron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
8.3field-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

35 citing papers in PubMed, 41 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

20 authors at 7 institutions in 4 countries.

Adekunle T BademosiVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium; Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St Lucia Campus, Brisbane, QLD 4072, Australia.
Marianna DecetVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Sabine KuenenVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Carles CalatayudVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Jef SwertsVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Sandra F GallegoVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Nils SchoovaertsVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium.
Spyridoula KaramanouKU Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven 3000, Belgium.
Nikolaos LourosVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; Switch Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven 3000, Belgium.
Ella MartinVIB-VUB Center for Structural Biology, Brussels 1050, Belgium; Department of Structural Biology Brussels, Vrije Universiteit Brussel, Brussels 1050, Belgium.
Jean-Baptiste SibaritaInterdisciplinary Institute for Neuroscience, University of Bordeaux, F-33000 Bordeaux, France.
Katlijn VintsVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium; VIB Bio Core, KU Leuven, Leuven 3000, Belgium.
Natalia V GounkoVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium; VIB Bio Core, KU Leuven, Leuven 3000, Belgium.
Frédéric A MeunierClem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, St Lucia Campus, Brisbane, QLD 4072, Australia; School of Biomedical Sciences, The University of Queensland, St Lucia Campus, Brisbane, QLD 4072, Australia.
Anastassios EconomouKU Leuven, Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven 3000, Belgium.
Wim VerséesVIB-VUB Center for Structural Biology, Brussels 1050, Belgium; Department of Structural Biology Brussels, Vrije Universiteit Brussel, Brussels 1050, Belgium.
Frederic RousseauVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; Switch Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven 3000, Belgium.
Joost SchymkowitzVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; Switch Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven 3000, Belgium.
Sandra-F SoukupUniv. Bordeaux, CNRS UMR 5293, F-33000 Bordeaux, France. Electronic address: soukuplab@gmail.com.
Patrik VerstrekenVIB-KU Leuven Center for Brain & Disease Research, Leuven 3000, Belgium; KU Leuven, Department of Neurosciences, Leuven Brain Institute, Mission Lucidity, Leuven 3000, Belgium. Electronic address: patrik.verstreken@kuleuven.be.
VIB-KU Leuven Center for Brain & Disease Research · BERega Institute for Medical Research · BEVrije Universiteit Brussel · BEAllen Institute for Brain Science · USCentre National de la Recherche Scientifique · FRThe University of Queensland · AUUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal activity causes use-dependent decline in protein function. However, it is unclear how this is coupled to local quality control mechanisms. We show in Drosophila that the endocytic protein Endophilin-A (EndoA) connects activity-induced calcium influx to synaptic autophagy and neuronal survival in a Parkinson disease-relevant fashion. Mutations in the disordered loop, including a Parkinson disease-risk mutation, render EndoA insensitive to neuronal stimulation and affect protein dynamics: when EndoA is more flexible, its mobility in membrane nanodomains increases, making it available for autophagosome formation. Conversely, when EndoA is more rigid, its mobility reduces, blocking stimulation-induced autophagy. Balanced stimulation-induced autophagy is required for dopagminergic neuron survival, and a variant in the human ENDOA1 disordered loop conferring risk to Parkinson disease also blocks nanodomain protein mobility and autophagy both in vivo and in human-induced dopaminergic neurons. Thus, we reveal a mechanism that neurons use to connect neuronal activity to local autophagy and that is critical for neuronal survival.

Indexed as

Parkinson DiseaseAcyltransferasesAdaptor Proteins, Signal TransducingAnimalsAutophagyCalciumDopaminergic NeuronsDrosophilaDrosophila ProteinsHumansMutationAcyltransferasesAdaptor Proteins, Signal TransducingCalciumDrosophila Proteinsendophilin A, DrosophilaSH3GL2 protein, humanCa(2+) influxendophilinAneuronal activityParkinson diseasesynaptic autophagy

Identifiers

PMID36827984
PMCPMC10166451
OpenAlexW4321613221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.