Evidence map›Paper›PMID 38323747›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Investigating alpha-synuclein co-pathology in Alzheimer's disease by means of cerebrospinal fluid alpha-synuclein seed amplification assay.

Giovanni Bellomo, Andrea Toja, Federico Paolini Paoletti, Yihua Ma, Carly M Farris, Lorenzo Gaetani, Nicola Salvadori, Davide Chiasserini, Anna Lidia Wojdaƚa, Luis Concha-Marambio and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
31.7field-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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Cross-disease protein aggregate interactions in neurodegeneration: from molecular mechanisms to therapeutic strategies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. ATNIVS biomarker heterogeneity in real-world patients receiving lecanemab.The journal of prevention of Alzheimer's disease · 2026
    Article
  13. Thalamic nuclei insights into Alzheimer's disease.bioRxiv : the preprint server for biology · 2026
    Article
  14. Effects of α-synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  15. Article
  16. Review
  17. Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  18. Article
  19. Article
  20. A Biomarker-Based Classification of Corticobasal Syndrome.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article

8 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 2 countries.

Giovanni BellomoCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0003-0456-5650
Andrea TojaCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0009-0000-9500-7632
Federico Paolini PaolettiCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0001-9623-1900
Yihua MaR&D Unit, Amprion Inc, San Diego, California, USA.
Carly M FarrisR&D Unit, Amprion Inc, San Diego, California, USA.ORCID 0000-0002-8277-8531
Lorenzo GaetaniCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0003-3967-8954
Nicola SalvadoriCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
Davide ChiasseriniSection of Physiology and Biochemistry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0002-1169-3258
Anna Lidia WojdaƚaCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0002-6958-8223
Luis Concha-MarambioR&D Unit, Amprion Inc, San Diego, California, USA.ORCID 0000-0002-9454-8389
Lucilla ParnettiCenter for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.ORCID 0000-0001-5722-3967
University of Perugia · ITAmprion (United States) · US

Funding

European Union-Next Generation EU PNRR-MAD-2022-12376035Marie Skłodowska-Curie actions 860197Michael J Fox Foundation MJFF-021233Parkinson's Foundation PF-PRF-934916
6 · The paper itself

Abstract

introductionLewy body disease, a frequently observed co-pathology in Alzheimer's disease (AD), can be identified antemortem in cerebrospinal fluid (CSF) by α-synuclein seed amplification assay (αS-SAA). The prevalence and clinical impact of CSF αS-SAA positivity in AD are still unknown.

methodsαS-SAA was performed on CSF samples from 240 AD patients (preclinical, prodromal, and dementia stages), 85 controls, 84 patients with Parkinson's disease (PD), and 21 patients with PD with dementia or dementia with Lewy bodies. In AD patients, associations between αS-SAA positivity and cognitive changes were also evaluated.

resultsIn agreement with available neuropathological studies, αS-SAA positivity was observed in 30% of AD patients (vs 9% in controls), and was associated with cognitive decline, visuospatial impairment, and behavioral disturbances. DISCUSSION: αS-SAA positivity in AD patients reflects the prevalence observed in neuropathological series and is associated with a worse clinical outcome. These data confirm the validity of CSF αS-SAA positivity as biomarker of synucleinopathy.

Indexed as

Alzheimer DiseaseLewy Body DiseaseParkinson DiseaseSynucleinopathiesalpha-SynucleinAmyloid beta-PeptidesBiomarkersHumanstau Proteinsalpha-SynucleinAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer's diseasebiomarkerscerebrospinal fluidneuropsychological evaluationseed amplification assaysynucleinopathy

Identifiers

PMID38323747
PMCPMC11032521
OpenAlexW4391614296

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.