Evidence map›Paper›PMID 26401929›Full record

ArticleJournal of Alzheimer's disease : JAD2015

Increased Number of Plasma B Cells Producing Autoantibodies Against Aβ42 Protofibrils in Alzheimer's Disease.

Sofia Söllvander, Frida Ekholm-Pettersson, Rose-Marie Brundin, Gabriel Westman, Lena Kilander, Staffan Paulie, Lars Lannfelt, Dag Sehlin

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
–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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  4. Article
  5. Article
  6. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
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  13. Amyloid-Related Imaging Abnormality (ARIA) Beyond the APOE-ε4 Allele.Chronic diseases and translational medicine · 2025
    Review
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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

8 authors.

Sofia SöllvanderDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Frida Ekholm-PetterssonDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Rose-Marie BrundinDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Gabriel WestmanDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Lena KilanderDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Staffan PaulieMabtech AB, Nacka Strand, Sweden.
Lars LannfeltDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Dag SehlinDepartment of Public Health & Caring Sciences/Molecular Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Alzheimer's disease (AD)-related peptide amyloid-β (Aβ) has a propensity to aggregate into various assemblies including toxic soluble Aβ protofibrils. Several studies have reported the existence of anti-Aβ antibodies in humans. However, it is still debated whether levels of anti-Aβ antibodies are altered in AD patients compared to healthy individuals. Formation of immune complexes with plasma Aβ makes it difficult to reliably measure the concentration of circulating anti-Aβ antibodies with certain immunoassays, potentially leading to an underestimation. Here we have investigated anti-Aβ antibody production on a cellular level by measuring the amount of anti-Aβ antibody producing cells instead of the plasma level of anti-Aβ antibodies. To our knowledge, this is the first time the anti-Aβ antibody response in plasma has been compared in AD patients and age-matched healthy individuals using the enzyme-linked immunospot (ELISpot) technique. Both AD patients and healthy individuals had low levels of B cells producing antibodies binding Aβ40 monomers, whereas the number of cells producing antibodies toward Aβ42 protofibrils was higher overall and significantly higher in AD compared to healthy controls. This study shows, by an alternative and reliable method, that there is a specific immune response to the toxic Aβ protofibrils, which is significantly increased in AD patients.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAutoantibodiesBiotinylationB-LymphocytesCase-Control StudiesEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansMaleMental Status SchedulePeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)AutoantibodiesPeptide FragmentsAmyloid-βamyloid-β protofibrilsanti-amyloid-β antibodiesenzyme-linked immunospot assay

Identifiers

PMID26401929
PMCPMC4923756

What OpenQuestion holds

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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.