Evidence map›Paper›PMID 40885755›Full record

ArticleNPJ Parkinson's disease2025

Elevated hexosylceramides in Parkinson's disease cause gene upregulations in neurons mimicking responses to pathogens.

Luisa Franck, Lisa Hahnefeld, Lucie Valek, Katharina Klatt-Schreiner, Annett Wilken-Schmitz, Mohamad Wessam Alnouri, Sandra Trautmann, Marc-Philipp Weyer, Dominique Thomas, Robert Gurke and 3 more

Abstract read
In one paragraph

Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Elevation of Stearoyl-Coenzyme A Desaturase and Monounsaturated Fatty Acids in Parkinson's Disease Serum.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  2. Article
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

13 authors.

Luisa FranckGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Lisa HahnefeldGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Lucie ValekGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Katharina Klatt-SchreinerGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Annett Wilken-SchmitzGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Mohamad Wessam AlnouriMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.
Sandra TrautmannGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Marc-Philipp WeyerGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Dominique ThomasGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Robert GurkeGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Stefan OffermannsMax Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.
Gerd GeisslingerGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany.
Irmgard TegederGoethe University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Frankfurt am Main, Germany. tegeder@em.uni-frankfurt.de.

Funding

Deutsche Forschungsgemeinschaft CRC1039 A03Deutsche Forschungsgemeinschaft, Germany CRC1039 A04Deutsche Forschungsgemeinschaft, Germany CRC1039 Z01
6 · The paper itself

Abstract

Parkinson's Disease (PD) is driven by pathological aggregates of alpha-synuclein (αSyn), whose formation is facilitated by impaired glycosphingolipid metabolism via acidic glucocerebrosidase (GCase). We investigated glucosylceramide (GlcCer) accumulation in human, mouse, and cellular PD models. Lipidomic analyses revealed elevated plasma GlcCer, especially GlcCer24:1, and a shift in phosphatidylcholine (PC) species in PD patients. PD patient skin fibroblasts accumulated more GlcCer under lysosomal stress. GlcCer and sulfatides (SHexCer) were increased in Pink1

Identifiers

PMID40885755
PMCPMC12398573

What OpenQuestion holds

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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.