Evidence map›Paper›PMID 29196815›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Amyloid β oligomers (AβOs) in Alzheimer's disease.

Barbara Mroczko, Magdalena Groblewska, Ala Litman-Zawadzka, Johannes Kornhuber, Piotr Lewczuk

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. The Tetrapeptide HAEE Promotes Amyloid-Beta Clearance from the Brain.International journal of molecular sciences · 2025
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  20. Common and Trace Metals in Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2023
    Review

20 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Barbara MroczkoDepartment of Neurodegeneration Diagnostics, Medical University of Białystok, Białystok, Poland.
Magdalena GroblewskaDepartment of Biochemical Diagnostics, University Hospital in Białystok, Białystok, Poland.
Ala Litman-ZawadzkaDepartment of Neurodegeneration Diagnostics, Medical University of Białystok, Białystok, Poland.
Johannes KornhuberLab for Clinical Neurochemistry and Neurochemical Dementia Diagnostics, Department of Psychiatry and Psychotherapy, Universitätsklinikum Erlangen, and Friedrich-Alexander Universität Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany.
Piotr LewczukDepartment of Neurodegeneration Diagnostics, Medical University of Białystok, Białystok, Poland. Piotr.Lewczuk@uk-erlangen.de.ORCID 0000-0002-8101-6535
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMedical University of Białystok · PLUniversity Clinical Hospital In Bialystok · PL

Funding

IMI 115372
6 · The paper itself

Abstract

The causative role of amyloid β 1-42 (Aβ42) aggregation in the pathogenesis of Alzheimer's disease (AD) has been under debate for over 25 years. Primarily, scientific efforts have focused on the dyshomeostasis between production and clearance of Aβ42. This imbalance may result from mutations either in genes for the substrate, i.e., amyloid precursor protein or in genes encoding presenilin, the enzyme of the reaction that generates Aβ42. Currently, it is supposed that soluble oligomers of amyloid beta (AβOs) and not fibrillar Aβ42 within neuritic plaques may be the toxic factors acting on a very early stage of AD, perhaps even initiating pathological cascade. For example, soluble AβOs isolated from AD patients' brains reduced number of synapses, inhibited long-term potentiation, and enhanced long-term synaptic depression in brain regions responsible for memory in animal models of AD. Concentrations of AβOs in the cerebrospinal fluid (CSF) of AD patients are often reported higher than in non-demented controls, and show a negative correlation with mini-mental state examination scores. Furthermore, increased Aβ42/oligomer ratio in the CSF of AD/MCI patients indicated that the presence of soluble AβOs in CSF may be linked to lowering of natively measured monomeric Aβ42 by epitopes masking, and hence, concentrations of AβOs in the CSF are postulated to as useful AD biomarkers.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersHumansPeptide FragmentsAmyloid beta-PeptidesBiomarkersPeptide FragmentsAlzheimer’s diseaseAmyloid-β oligomerBiomarkersCerebrospinal fluidNeurodegenerationProtein aggregation

Identifiers

PMID29196815
OpenAlexW2774913139

What OpenQuestion holds

Textmetadata
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.