Evidence map›Paper›PMID 38242875›Full record

ArticleNPJ Parkinson's disease2024

CSF α-synuclein seed amplification kinetic profiles are associated with cognitive decline in Parkinson's disease.

Kathrin Brockmann, Stefanie Lerche, Simone Baiardi, Marcello Rossi, Isabel Wurster, Corinne Quadalti, Benjamin Roeben, Angela Mammana, Milan Zimmermann, Ann-Kathrin Hauser and 5 more

Open access · goldAbstract read
In one paragraph

Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
19.9field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

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  8. Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  13. Lewy body dementia promotion by air pollutants.Science (New York, N.Y.) · 2025
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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

15 authors at 2 institutions in 3 countries.

Kathrin BrockmannDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany. kathrin.brockmann@uni-tuebingen.de.ORCID http://orcid.org/0000-0002-7515-8596
Stefanie LercheDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.ORCID http://orcid.org/0000-0002-5508-004X
Simone BaiardiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Marcello RossiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Isabel WursterDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.
Corinne QuadaltiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.ORCID http://orcid.org/0000-0002-0302-3027
Benjamin RoebenDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.ORCID http://orcid.org/0000-0002-4905-8698
Angela MammanaIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Milan ZimmermannDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.
Ann-Kathrin HauserDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.
Christian DeuschleDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.
Claudia SchulteDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.
Inga Liepelt-ScarfoneGerman Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Thomas GasserDepartment of Neurodegeneration, Center of Neurology, Hertie Institute for Clinical Brain Research, German Center for Neurodegenerative Diseases, University of Tuebingen, Hoppe Seyler‑Strasse 3, 72076, Tuebingen, Germany.ORCID http://orcid.org/0000-0002-1069-1146
Piero ParchiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.ORCID http://orcid.org/0000-0002-9444-9524
German Center for Neurodegenerative Diseases · DEIstituto delle Scienze Neurologiche di Bologna · IT

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) PDStratMichael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation) Prevent demetia in GBA-associated PDRegione Emilia-Romagna (Emilia-Romagna Region) FIN-RER 2020
6 · The paper itself

Abstract

Seed amplification assays have been implemented in Parkinson's disease to reveal disease-specific misfolded alpha-synuclein aggregates in biospecimens. While the assays' qualitative dichotomous seeding response is valuable to stratify and enrich cohorts for alpha-synuclein pathology in general, more quantitative parameters that are associated with clinical dynamics of disease progression and that might potentially serve as exploratory outcome measures in clinical trials targeting alpha-synuclein would add important information. To evaluate whether the seeding kinetic parameters time required to reach the seeding threshold (LAG phase), the peak of fluorescence response (Imax), and the area under the curve (AUC) are associated with clinical trajectories, we analyzed LAG, Imax, and AUC in relation to the development of cognitive decline in a longitudinal cohort of 199 people with Parkinson's disease with positive CSF alpha-synuclein seeding status. Patients were stratified into tertiles based on their individual CSF alpha-synuclein seeding kinetic properties. The effect of the kinetic parameters on longitudinal development of cognitive impairment defined by MoCA ≤25 was analyzed by Cox-Regression. Patients with a higher number of positive seeding replicates and tertile groups of shorter LAG, higher Imax, and higher AUC showed a higher prevalence of and a shorter duration until cognitive impairment longitudinally (3, 6, and 3 years earlier with p ≤ 0.001, respectively). Results remained similar in separate subgroup analyses of patients with and without GBA mutation. We conclude that a more prominent alpha-synuclein seeding kinetic profile translates into a more rapid development of cognitive decline.

Identifiers

PMID38242875
PMCPMC10799016
OpenAlexW4391042194

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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.