Evidence map›Paper›PMID 40051075›Full record

ArticleAnnals of clinical and translational neurology2025

Relationship of cognitive decline with glucocerebrosidase activity and amyloid-beta 42 in DLB and PD.

Maria Camila Gonzalez, Linn Oftedal, Johannes Lange, Diego Alejandro Tovar-Rios, Ole-Bjørn Tysnes, Claire Paquet, Marta Marquié, Mercè Boada, Daniel Alcolea, Konrad Rejdak and 6 more

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 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. Article
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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

16 authors.

Maria Camila GonzalezDepartment of Quality and Health Technology, Faculty of Health Sciences, University of Stavanger, Stavanger, Norway.ORCID 0000-0003-1061-4164
Linn OftedalCentre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway.
Johannes LangeCentre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway.
Diego Alejandro Tovar-RiosDepartment of Quality and Health Technology, Faculty of Health Sciences, University of Stavanger, Stavanger, Norway.
Ole-Bjørn TysnesDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.
Claire PaquetNeurology Center, Assistance Publique Hôpitaux de Paris, Lariboisière Fernand-Widal Hospital, INSERMU1144, Université de Paris, Paris, France.
Marta MarquiéAce Alzheimer Center Barcelona-Universitat Internacional de Catalunya, Barcelona, Spain.
Mercè BoadaAce Alzheimer Center Barcelona-Universitat Internacional de Catalunya, Barcelona, Spain.
Daniel AlcoleaSant Pau Memory Unit, Department of Neurology, IIB Sant Pau-Hospital de Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.ORCID 0000-0002-3819-3245
Konrad RejdakDepartment of Neurology, Medical University of Lublin, Lublin, Poland.
Ewa PapucDepartment of Neurology, Medical University of Lublin, Lublin, Poland.
Jakub HortDepartment of Neurology, Memory Clinic, Charles University, Second Faculty of Medicine and Motol University Hospital, Prague, Czech Republic.
Cristian Falup-PecurariuDepartment of Neurology, County Clinic Hospital, Faculty of Medicine, Transilvania University, Brasov, Romania.
Dag AarslandCentre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.
Guido AlvesCentre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway.
Jodi Maple-GrødemCentre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway.

Funding

Departament de Salut, Generalitat de Catalunya PERIS program SLT006/17/125Instituto de Salud Carlos III INT19/00016Instituto de Salud Carlos III INT23/00048Instituto de Salud Carlos III PI18/00435Instituto de Salud Carlos III PI22/00611Next Generation EU LX22NPO5107 MEYSResearch Council of Norway 177966Western Norway Regional Health Authority 911218Western Norway Regional Health Authority 911949
6 · The paper itself

Abstract

objectiveDementia with Lewy bodies (DLB) and Parkinson's disease (PD) share clinical, pathological, and genetic risk factors, including GBA1 and APOEε4 mutations. Biomarkers associated with the pathways of these mutations, such as glucocerebrosidase enzyme (GCase) activity and amyloid-beta 42 (Aβ42) levels, may hold potential as predictive indicators, providing valuable insights into the likelihood of cognitive decline within these diagnoses. Our objective was to determine their association with cognitive decline in DLB and PD.

methodsA total of 121 DLB patients from the European-DLB Consortium and 117 PD patients from the Norwegian ParkWest Study were included in this study. The four most commonly associated variants of GBA1 mutations (E326K, T369M, N370S, L444P), APOEε4 status, and cerebrospinal fluid (CSF) Aβ42 levels and GCase activity were assessed, as well as global cognition using the Mini-Mental State Examination. Linear mixed-effects regression models were used to evaluate the association of CSF biomarkers with cognitive decline in each diagnostic group, adjusted for age, sex, education, and genetic mutation profile.

resultsLow CSF Aβ42 levels were associated with accelerated cognitive decline in DLB, whereas reduced CSF GCase activity predicted faster cognitive decline in PD. These associations were independent of GBA1 gene mutations or APOEε4 status.

interpretationOur study provides important evidence on the relationship between brain Aβ deposition and GCase activity in the Lewy body disease spectrum independent of their genetic mutation profile. This information could be relevant for designing future clinical trials targeting these pathways.

Indexed as

Amyloid beta-PeptidesCognitive DysfunctionGlucosylceramidaseLewy Body DiseaseParkinson DiseasePeptide FragmentsAgedAged, 80 and overBiomarkersFemaleHumansMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersGBA protein, humanGlucosylceramidasePeptide Fragments

Identifiers

PMID40051075
PMCPMC12093344

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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.