Evidence map›Paper›PMID 41980956›Full record

ArticleNPJ Parkinson's disease2026

Clinical correlates of a negative cerebrospinal fluid α-synuclein seed amplification assay result in Parkinson's disease.

Andrea Mastrangelo, Isabel Wurster, Alice Ticca, Stefanie Lerche, Corrado Zenesini, Benjamin Röben, Angela Mammana, Ann-Kathrin Hauser, Edoardo Ruggeri, Christian Deuschle and 6 more

Abstract read
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In one paragraph

Article in NPJ Parkinson's disease, 2026. 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. Review
  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

16 authors.

Andrea MastrangeloDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Isabel WursterDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Alice TiccaDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Stefanie LercheDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Corrado ZenesiniIRCCS, Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
Benjamin RöbenDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Angela MammanaIRCCS, Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
Ann-Kathrin HauserDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Edoardo RuggeriIRCCS, Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
Christian DeuschleDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Erica VittoriosiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Giuseppe Mario BentivengaDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Claudia SchulteDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Sabina CapellariDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Kathrin BrockmannDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany. kathrin.brockmann@uni-tuebingen.de.
Piero ParchiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy. piero.parchi@unibo.it.

Funding

Bundesministerium für Bildung und Forschung PDdementiaDeutsches Zentrum für Neurodegenerative Erkrankungen PD research; MIGAP studyMinistero della Salute RF-2021-12374386 and "Ricerca Corrente"Ministero dell'Università e della Ricerca project MNESYS (PE0000006)
6 · The paper itself

Abstract

We investigated the basis and clinical correlates of a negative cerebrospinal fluid (CSF) alpha-synuclein (α-syn) seed amplification assay result in patients with a clinical diagnosis of sporadic or GBA1-associated PD formulated by movement disorder specialists. Out of 473 participants with a confirmed PD diagnosis at the last follow-up, 62 (13.1%) were α-syn negative. Among them, 3 out of 15 with available longitudinal CSF samples converted to α-syn positive. Alpha-syn negative participants had more severe axial motor impairment, lower odds of hyposmia, REM sleep behaviour disorder and constipation. There were no differences in motor and cognitive progression between groups. CSF neurofilament light chain values were not associated with α-syn status. Besides possible misdiagnosis, the results indicate that α-syn negative PD comprises a distinct patient subgroup, possibly associated with a low burden or absence of Lewy body pathology. The results support the use of CSF α-syn SAA in PD patient stratification.

Identifiers

PMID41980956
PMCPMC13086934

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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.