Evidence map›Paper›PMID 30413735›Full record

ArticleScientific reports2018

Amyloid precursor protein-fragments-containing inclusions in cardiomyocytes with basophilic degeneration and its association with cerebral amyloid angiopathy and myocardial fibrosis.

Lara Maria Krämer, Johannes Brettschneider, Jochen K Lennerz, Daniel Walcher, Lubin Fang, Angela Rosenbohm, Karthikeyan Balakrishnan, Julian Benckendorff, Peter Möller, Steffen Just and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Effects ofMolecules (Basel, Switzerland) · 2026
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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

13 authors at 5 institutions in 4 countries.

Lara Maria KrämerInstitute of Pathology, Ulm University, Ulm, Germany.
Johannes BrettschneiderRehaClinic Lucerne, Lucerne, Switzerland.
Jochen K LennerzInstitute of Pathology, Ulm University, Ulm, Germany.
Daniel WalcherDepartment of Internal Medicine II (Cardiology), Ulm University, Ulm, Germany.
Lubin FangDepartment of Neurology, Ulm University, Ulm, Germany.
Angela RosenbohmDepartment of Neurology, Ulm University, Ulm, Germany.
Karthikeyan BalakrishnanInstitute of Pathology, Ulm University, Ulm, Germany.
Julian BenckendorffInstitute of Pathology, Ulm University, Ulm, Germany.
Peter MöllerInstitute of Pathology, Ulm University, Ulm, Germany.
Steffen JustDepartment of Internal Medicine II (Cardiology), Ulm University, Ulm, Germany.
Michael WillemBiomedical Center, Ludwig-Maximilians-Universität Munich, Munich, Germany.
Albert C LudolphDepartment of Neurology, Ulm University, Ulm, Germany.
Dietmar Rudolf ThalInstitute of Pathology, Ulm University, Ulm, Germany. dietmar.thal@kuleuven.be.ORCID http://orcid.org/0000-0002-1036-1075
Universität Ulm · DEAllen Institute for Brain Science · USHarvard University · USLudwig-Maximilians-Universität München · DEUniversity of Lucerne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiomyopathies with intracellular inclusions are a distinct subset of cardiomyopathies whereas basophilic degeneration (BD) of the heart describes inclusions in cardiomyocytes of the aging heart, which have not yet been related to a specific disease condition or to a distinct type of protein inclusion. To address the question whether BD represents a specific pathological feature and whether it is linked to a distinct disease condition we studied 62 autopsy cases. BD inclusions exhibited an immunohistochemical staining pattern related to glycosylated, δ- or η-secretase-derived N-terminal cleavage products of the amyloid precursor protein (sAPPδ/η) or shorter fragments of sAPPη. BD aggregates were found in the myocardium of both ventricles and atria with highest amounts in the atria and lowest in the interventricular septum. The frequency of BD-lesions correlated with age, degree of myocardial fibrosis in individuals with arterial hypertension, and the severity of cerebral amyloid angiopathy (CAA). The intracytoplasmic deposition of N-terminal sAPPδ/η fragments in BD indicates a specific inclusion body pathology related to APP metabolism. The correlation with the severity of CAA, which is related to the APP-derived amyloid β-protein, supports this point of view and suggests a possible link between myocardial and cerebrovascular APP-related lesions.

Indexed as

Inclusion BodiesAdolescentAdultAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCardiomyopathiesCerebral Amyloid AngiopathyChildChild, PreschoolFemaleFibrosisHumansInfantAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, human

Identifiers

PMID30413735
PMCPMC6226444
OpenAlexW2899621494

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.