Evidence map›Paper›PMID 40874677›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Alzheimer's disease traits in Parkinson's disease without α-synuclein seeding.

Bárbara Fernandes Gomes, Carly M Farris, Yihua Ma, Luis Concha-Marambio, Johanna Nilsson, Karin Forsberg, Russ Lebovitz, Ulf Andreasson, Kaj Blennow, Henrik Zetterberg and 1 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Alzheimer's disease traits in Parkinson's disease without α-synuclein seeding.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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

11 authors.

Bárbara Fernandes GomesDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID 0000-0002-1512-6699
Carly M FarrisR&D Unit, Amprion Inc., San Diego, California, USA.
Yihua MaR&D Unit, Amprion Inc., San Diego, California, USA.
Luis Concha-MarambioR&D Unit, Amprion Inc., San Diego, California, USA.
Johanna NilssonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Karin ForsbergDepartment of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.
Russ LebovitzR&D Unit, Amprion Inc., San Diego, California, USA.
Ulf AndreassonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
David BäckströmDepartment of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.

Funding

AD Strategic FundAD Strategic Fund and the Alzheimer's AssociationAlzheimer's Association #ADSF-21-831376-CAlzheimer's Association #ADSF-21-831377-CAlzheimer's Association #ADSF-21-831381-CAlzheimer's Association #ADSF-24-1284328-CAlzheimer's Association 2021 Zenith AwardAlzheimer's Association 2022-2025 GrantAlzheimer's Drug Discovery Foundation 201809-2016862Bluefield ProjectCare Research University College London Hospitals Biomedical Research CentreCopenhagenCure Alzheimer's FundErling-Persson FoundationEU Joint Programme - Neurodegenerative Disease Research JPND2019-466-236European Partnership on MetrologyEuropean Research CouncilEuropean Union Joint Programme - Neurodegenerative Disease Research JPND2021-00694European Union's HorizonFamiljen Rönströms StiftelseFondation Générale de SantéH2020 European Research CouncilH2020 Marie Skłodowska-Curie Actions 860197HjärnfondenHjärnfonden, Sweden #ALFGBG-715986Hjärnfonden, Sweden #ALFGBG-965240Hjärnfonden, Sweden #ALZ2022-0006Hjärnfonden, Sweden #FO2017-0243Hjärnfonden, Sweden JPND2019-466-236Hjärnfonden, Sweden SG-23-1038904 QCHjärnfonden, Sweden ZEN-21-848495HORIZON EUROPE Reforming and enhancing the European Research and Innovation system 101053962Kempe FoundationKempestiftelsernaKirsten and Freddy Johansen FoundationKirsten og Freddy Johansens FondMichael J. Fox Foundation for Parkinson's Research MJFF-021233National Institute for HealthNational Institute for Health and Care Research University College London Hospitals Biomedical Research CentreOlav Thon FoundationOlav Thon StiftelsenParkinsonfondenParkinsonFörbundetParkinson Research FoundationParticipating States #22HLT07Stiftelsen för Gamla TjänarinnorSwedish Alzheimer Foundation #AF-930351Swedish Alzheimer Foundation #AF-939721Swedish Alzheimer Foundation #AF-968270Swedish Alzheimer Foundation #AF-994551Swedish Medical Research CouncilSwedish Parkinson FoundationSwedish PD AssociationSwedish Research Council 101053962Swedish Research Council #2019-02397Swedish Research Council #2022-01018Swedish Research Council #2023-00356Swedish State Support for Clinical Research #ALFGBG-71320The Bluefield ProjectThe Familjen Erling-Perssons StiftelseUK Dementia Research Institute #2017-00915UK Dementia Research Institute #2022-00732UK Dementia Research Institute UKDRI-1003Umeå UniversitetVästerbotten Läns Landsting
6 · The paper itself

Abstract

introductionThe α-synuclein (αSyn) seed amplification assay (αSyn-SAA) is an accurate tool to detect αSyn seeds in patients with Parkinson's disease (PD). However, a minority of clinically diagnosed PD patients are negative for αSyn.

methodsThe αSyn-SAA was performed in cerebrospinal fluid (CSF) of individuals with PD (n = 93), multiple system atrophy (MSA, n = 26), progressive supranuclear palsy (PSP, n = 18), corticobasal syndrome (n = 3), and healthy controls (n = 29).

resultsThe αSyn-SAA detected αSyn in 90% of PD and 81% of MSA patients, while exhibiting high specificity (97%). SAA- PD patients had a distinct phenotype compared to SAA+ PD, including a marked postural instability/gait disorder (P = 0.002), impaired episodic memory, and lower CSF amyloid beta DISCUSSION: A negative αSyn-SAA in PD is associated with a distinct phenotype and pathological findings suggesting that these patients may have a motor subtype of Alzheimer's disease. This could influence future clinical trials. HIGHLIGHTS: The α-synuclein seed amplification assay (αSyn-SAA) is a robust assay. αSyn-SAA-negative Parkinson's disease shows a distinct motor-cognitive phenotype. Autopsy showed Alzheimer's disease (AD) pathology in parkinsonian diseases. AD stands as a major clinical confounder for the diagnosis of movement disorders.

Indexed as

alpha-SynucleinAlzheimer DiseaseParkinson DiseaseAgedAmyloid beta-PeptidesBiomarkersFemaleHumansMaleMiddle AgedMultiple System AtrophySupranuclear Palsy, Progressivealpha-SynucleinAmyloid beta-PeptidesBiomarkersAlzheimer's diseasefluid biomarkerParkinson's diseaseseed amplification assaysynucleinopathy

Identifiers

PMID40874677
PMCPMC12086808

What Socratic holds

Textmetadata
LicenceCC BY
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.