Evidence map›Paper›PMID 28994710›Full record

ArticleMolecules (Basel, Switzerland)2017

Large-Scale Oral Treatment Study with the Four Most Promising D3-Derivatives for the Treatment of Alzheimer's Disease.

Janine Kutzsche, Sarah Schemmert, Markus Tusche, Jörg Neddens, Roland Rabl, Dagmar Jürgens, Oleksandr Brener, Antje Willuweit, Birgit Hutter-Paier, Dieter Willbold

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  3. The N-type calcium channel rises from the ashes.The Journal of clinical investigation · 2025
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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

10 authors at 3 institutions in 2 countries.

Janine KutzscheInstitute of Complex Systems, Structural Biochemistry (ICS-6), Forschungszentrum Jülich, Jülich 52425, Germany. j.kutzsche@fz-juelich.de.
Sarah SchemmertInstitute of Complex Systems, Structural Biochemistry (ICS-6), Forschungszentrum Jülich, Jülich 52425, Germany. s.schemmert@fz-juelich.de.
Markus TuscheInstitute of Complex Systems, Structural Biochemistry (ICS-6), Forschungszentrum Jülich, Jülich 52425, Germany. m.tusche@fz-juelich.de.
Jörg NeddensQPS Austria GmbH, Grambach A-8074, Austria. joerg.neddens@qps.com.
Roland RablQPS Austria GmbH, Grambach A-8074, Austria. roland.rabl@qps.com.
Dagmar JürgensInstitute of Complex Systems, Structural Biochemistry (ICS-6), Forschungszentrum Jülich, Jülich 52425, Germany. d.juergens@fz-juelich.de.
Oleksandr BrenerInstitut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf 40225, Germany. brener@biophys.uni-duesseldorf.de.
Antje WilluweitInstitute of Neuroscience and Medicine, Medical Imaging Physics (INM-4), Forschungszentrum Jülich, Jülich 52425, Germany. a.willuweit@fz-juelich.de.ORCID 0000-0002-6725-0755
Birgit Hutter-PaierQPS Austria GmbH, Grambach A-8074, Austria. birgit.hutter-paier@qps.com.
Dieter WillboldInstitute of Complex Systems, Structural Biochemistry (ICS-6), Forschungszentrum Jülich, Jülich 52425, Germany. d.willbold@fz-juelich.de.
Forschungszentrum Jülich · DEQPS (Austria) · ATHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is associated with the aggregation of the amyloid β protein (Aβ). Aβ oligomers are currently thought to be the major neurotoxic agent responsible for disease development and progression. Thus, their elimination is highly desirable for therapy development. Our therapeutic approach aims at specific and direct elimination of toxic Aβ oligomers by stabilizing Aβ monomers in an aggregation-incompetent conformation. We have proven that our lead compound "D3", an all d-enantiomeric-peptide, specifically eliminates Aβ oligomers in vitro. In vivo, D3 enhances cognition and reduces plaque load in several transgenic AD mouse models. Here, we performed a large-scale oral proof of concept efficacy study, in which we directly compared four of the most promising D3-derivatives in transgenic mice expressing human amyloid precursor protein with Swedish and London mutations (APP

Indexed as

Administration, OralAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCell LineCell SurvivalCognition DisordersFemaleHumansMice, TransgenicMolecular StructureOligopeptidesPlaque, AmyloidProof of Concept StudyProtein Aggregation, PathologicalAmyloid beta-PeptidesAmyloid beta-Protein PrecursorD3 peptideOligopeptidesAlzheimer’s diseaseamyloid βAβ oligomerscognition">d-enantiomeric peptideslarge-scaleoral treatmenttransgenic mice

Identifiers

PMID28994710
PMCPMC6151452
OpenAlexW2763413361

What OpenQuestion 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 OpenQuestion graph.