Evidence map›Paper›PMID 40928027›Full record

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

Familial Alzheimer's disease mutation identifies novel role of SORLA in release of neurotrophic exosomes.

Kristian Juul-Madsen, Ina-Maria Rudolph, Jemila P Gomes, Katrina Meyer, Peter L Ovesen, Malgorzata Gorniak-Walas, Marianna Kokoli, Narasimha S Telugu, Malthe von Tangen Sivertsen, Fabia Febbraro and 6 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 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. Article
  2. Familial Alzheimer's disease mutation identifies novel role of SORLA in release of neurotrophic exosomes.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

16 authors.

Kristian Juul-MadsenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0002-5309-5221
Ina-Maria RudolphMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-3903-0755
Jemila P GomesMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0009-0004-1027-8599
Katrina MeyerMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-8244-6887
Peter L OvesenMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0001-8801-4711
Malgorzata Gorniak-WalasDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0003-1236-8622
Marianna KokoliMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-1411-3730
Narasimha S TeluguTechnology Platform for Pluripotent Stem Cells, Max Delbrueck Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0003-4509-7056
Malthe von Tangen SivertsenInterdisiciplinary Nanoscience Center, Aarhus University, Aarhus, Denmark.
Fabia FebbraroDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0001-8336-2776
Duncan S SutherlandInterdisiciplinary Nanoscience Center, Aarhus University, Aarhus, Denmark.ORCID 0000-0002-5045-9915
Johan PalmfeldtDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0001-5585-639X
Sebastian DieckeTechnology Platform for Pluripotent Stem Cells, Max Delbrueck Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-5219-5992
Olav M AndersenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0003-4226-3354
Matthias SelbachMax-Delbrueck-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0003-2454-8751
Thomas E WillnowDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0001-9515-7921

Funding

Alzheimer Forschung Initiative #18003Lundbeck Foundation R380-2021-1326Novo Nordisk Foundation NNF18OC0033928
6 · The paper itself

Abstract

introductionMutations in SORL1, encoding the sorting receptor Sortilin-related receptor with A-type repeats (SORLA), are found in individuals with Alzheimer's disease (AD). We studied SORLA

methodsWe investigated consequences of SORLA

resultsWe identified alterations in the SORLA DISCUSSION: We identified a role for SORLA in controlling quantity and neurotrophic quality of exosomes secreted by cells, suggesting impaired cellular cross talk through exosomes as a pathological trait contributing to AD pathology in carriers of SORL1 variants. HIGHLIGHTS: Familial Alzheimer's disease mutation in SORL1 changes interactome of mutant Sortilin-related receptor with A-type repeats (SORLA). Mutant SORLA impairs release of exosomes from neurons and microglia. Mutant exosomes lack neurotrophic qualities. Defect linked to alterations in microRNA content.

Indexed as

Alzheimer DiseaseExosomesLDL-Receptor Related ProteinsMembrane Transport ProteinsMutationHumansInduced Pluripotent Stem CellsMicrogliaMicroRNAsNeuronsLDL-Receptor Related ProteinsMembrane Transport ProteinsMicroRNAsSORL1 protein, humanAlzheimer's diseaseexosomesiPSC modelsmicrogliamulti‐omics

Identifiers

PMID40928027
PMCPMC12421412

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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.