Evidence map›Paper›PMID 42811169›Full record

ArticleEMBO reports2026

Condensate-driven triglyceride reduction links α-synuclein to mitochondrial dysfunction.

Tao Zhang, Alejandro Herron-Bedoya, María Eugenia Goya, Jorien C van der Weerd, Dikaia Tsagkari, Suzanne Couzijn, Lale Güngördü, Anna P Ainslie, Renée I Seinstra, M Rebecca Heiner Fokkema and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Tao ZhangEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. t.zhang@mail.hzau.edu.cn.ORCID http://orcid.org/0000-0001-8653-5089
Alejandro Herron-BedoyaEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
María Eugenia GoyaEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Jorien C van der WeerdDepartment of Laboratory Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Dikaia TsagkariInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Greece.ORCID http://orcid.org/0000-0003-1071-8203
Suzanne CouzijnEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0002-1449-9637
Lale GüngördüEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Anna P AinslieEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Renée I SeinstraEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0001-5083-399X
M Rebecca Heiner FokkemaDepartment of Laboratory Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0002-3477-0770
Ming ChangState Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China.
Nektarios TavernarakisInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Greece.ORCID http://orcid.org/0000-0002-5253-1466
Folkert KuipersEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.ORCID http://orcid.org/0000-0003-2518-737X
Ellen A A NollenEuropean Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. e.a.a.nollen@umcg.nl.ORCID http://orcid.org/0000-0003-3740-6373

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
European Commission Research Executive Agency Excellence Hub "CHAngeing" GA-101087071General Secretariat for Research and Innovation of the Greek Ministry of Development, the European Union - NextGenerationEU TAEDR-0535850Hellenic Foundation for Research and Innovation (H.F.R.I.) HFRI-FM17C3-0869HORIZON-WIDERA-2023-ACCESS-02 101159690Marie Sklodowska-Curie Gant Agreement 812830MOST | National Natural Science Foundation of China (NSFC) 32402082MSD co-funded by PPP Allowance awarded by Health~Holland LKR201161 MSD ERIBANIH Office of Research Infrastructure Programs P40 OD010440Stichting ParkinsonFonds 1887Stichting ParkinsonFonds 1907
6 · The paper itself

Abstract

α-Synuclein (αSyn) inclusions characterize multiple age-related neurodegenerative diseases, including Parkinson's disease (PD). While interactions between αSyn and lipids are known to contribute to αSyn pathobiology, the precise cellular mechanisms linking lipids to αSyn toxicity have yet to be elucidated. Through lipidomic profiling of Caenorhabditis elegans, we find that αSyn progressively alters lipid metabolism in aging worms. αSyn reduces the overall content of triacylglycerols (TAG) and disrupts the structure of lipid droplets (LD) and mitochondria. These pathological changes depend on αSyn's properties to bind lipid and to condensate into inclusions. Apart from lowering TAG levels, αSyn proportionally increases long-chain unsaturated fatty acids (LCUFAs). Consequently, genetic inhibition of LCUFA biosynthesis alleviates αSyn-induced loss of C. elegans motility. Supplementing Medium-Chain Triglyceride (MCT) on the other hand also improves αSyn-associated toxicity phenotypes. These results link αSyn lipid binding and condensation to impaired TAG metabolism, which drives cellular toxicity. Combined with observed lower plasma TAGs in Parkinson cohorts, our findings reveal contributions of TAG remodelling to αSyn toxicity and point at MCT-supplementation as a mechanism-based therapeutic opportunity in age-related synucleinopathies.

Identifiers

PMID42811169

What Socratic holds

Textmetadata
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 Socratic graph.