Evidence map›Paper›PMID 25143621›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Amyloid-β-induced action potential desynchronization and degradation of hippocampal gamma oscillations is prevented by interference with peptide conformation change and aggregation.

Firoz Roshan Kurudenkandy, Misha Zilberter, Henrik Biverstål, Jenny Presto, Dmytro Honcharenko, Roger Strömberg, Jan Johansson, Bengt Winblad, André Fisahn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. A Systematic Review of the Effects of Capsaicin on Alzheimer's Disease.International journal of molecular sciences · 2023
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Lateral Piezoelectricity of Alzheimer's Aβ Aggregates.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Review
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6 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

9 authors at 4 institutions in 4 countries.

Firoz Roshan KurudenkandyNeuronal Oscillations Laboratory, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and.
Misha ZilberterNeuronal Oscillations Laboratory, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and.
Henrik BiverstålCenter for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and.
Jenny PrestoCenter for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and.
Dmytro HoncharenkoDepartment of Biosciences and Nutrition, Karolinska Institutet, 17177 Stockholm, Sweden.
Roger StrömbergDepartment of Biosciences and Nutrition, Karolinska Institutet, 17177 Stockholm, Sweden.
Jan JohanssonCenter for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, The Biomedical Centre, 75123 Uppsala, Sweden, and Institute of Mathematics and Natural Sciences, Tallinn University, 10120 Tallinn, Estonia.
Bengt WinbladCenter for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and.
André FisahnNeuronal Oscillations Laboratory, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, and andre.fisahn@ki.se.
Alzheimer Society of Canada · CAKarolinska Institutet · SEAlzheimer's Society · GBSwedish University of Agricultural Sciences · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amyloid-β hypothesis of Alzheimer's Disease (AD) focuses on accumulation of amyloid-β peptide (Aβ) as the main culprit for the myriad physiological changes seen during development and progression of AD including desynchronization of neuronal action potentials, consequent development of aberrant brain rhythms relevant for cognition, and final emergence of cognitive deficits. The aim of this study was to elucidate the cellular and synaptic mechanisms underlying the Aβ-induced degradation of gamma oscillations in AD, to identify aggregation state(s) of Aβ that mediate the peptides neurotoxicity, and to test ways to prevent the neurotoxic Aβ effect. We show that Aβ(1-42) in physiological concentrations acutely degrades mouse hippocampal gamma oscillations in a concentration- and time-dependent manner. The underlying cause is an Aβ-induced desynchronization of action potential generation in pyramidal cells and a shift of the excitatory/inhibitory equilibrium in the hippocampal network. Using purified preparations containing different aggregation states of Aβ, as well as a designed ligand and a BRICHOS chaperone domain, we provide evidence that the severity of Aβ neurotoxicity increases with increasing concentration of fibrillar over monomeric Aβ forms, and that Aβ-induced degradation of gamma oscillations and excitatory/inhibitory equilibrium is prevented by compounds that interfere with Aβ aggregation. Our study provides correlative evidence for a link between Aβ-induced effects on synaptic currents and AD-relevant neuronal network oscillations, identifies the responsible aggregation state of Aβ and proofs that strategies preventing peptide aggregation are able to prevent the deleterious action of Aβ on the excitatory/inhibitory equilibrium and on the gamma rhythm.

Indexed as

Action PotentialsAmyloid beta-PeptidesAnimalsBiological ClocksCA3 Region, HippocampalExcitatory Amino Acid AgonistsFemaleIn Vitro TechniquesKainic AcidMaleMiceMice, Inbred C57BLNerve NetNeuronsPatch-Clamp TechniquesPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Excitatory Amino Acid AgonistsKainic AcidPeptide FragmentsProtein AggregatesAlzheimer's diseaseamyloid-β peptideBRICHOS domaingamma oscillationshippocampusneuronal synchronization

Identifiers

PMID25143621
PMCPMC6615507
OpenAlexW1967028445

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.