Evidence map›Paper›PMID 28938009›Full record

ArticlePLoS computational biology2017

Altering neuronal excitability to preserve network connectivity in a computational model of Alzheimer's disease.

Willem de Haan, Elisabeth C W van Straaten, Alida A Gouw, Cornelis J Stam

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. A complex network perspective on brain disease.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  3. Excitation-inhibition homeostasis in Alzheimer's disease: a selective multiscale review of mechanisms, sex differences, and therapeutic opportunities.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  4. Article
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  8. A Shift Toward Supercritical Brain Dynamics Predicts Alzheimer's Disease Progression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
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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

4 authors at 2 institutions in 1 country.

Willem de HaanDepartment of Clinical Neurophysiology and MEG, VUmc, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0003-3876-1764
Elisabeth C W van StraatenDepartment of Clinical Neurophysiology and MEG, VUmc, Amsterdam, The Netherlands.
Alida A GouwDepartment of Clinical Neurophysiology and MEG, VUmc, Amsterdam, The Netherlands.
Cornelis J StamDepartment of Clinical Neurophysiology and MEG, VUmc, Amsterdam, The Netherlands.
Amsterdam Neuroscience · NLAmsterdam UMC Location Vrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal hyperactivity and hyperexcitability of the cerebral cortex and hippocampal region is an increasingly observed phenomenon in preclinical Alzheimer's disease (AD). In later stages, oscillatory slowing and loss of functional connectivity are ubiquitous. Recent evidence suggests that neuronal dynamics have a prominent role in AD pathophysiology, making it a potentially interesting therapeutic target. However, although neuronal activity can be manipulated by various (non-)pharmacological means, intervening in a highly integrated system that depends on complex dynamics can produce counterintuitive and adverse effects. Computational dynamic network modeling may serve as a virtual test ground for developing effective interventions. To explore this approach, a previously introduced large-scale neural mass network with human brain topology was used to simulate the temporal evolution of AD-like, activity-dependent network degeneration. In addition, six defense strategies that either enhanced or diminished neuronal excitability were tested against the degeneration process, targeting excitatory and inhibitory neurons combined or separately. Outcome measures described oscillatory, connectivity and topological features of the damaged networks. Over time, the various interventions produced diverse large-scale network effects. Contrary to our hypothesis, the most successful strategy was a selective stimulation of all excitatory neurons in the network; it substantially prolonged the preservation of network integrity. The results of this study imply that functional network damage due to pathological neuronal activity can be opposed by targeted adjustment of neuronal excitability levels. The present approach may help to explore therapeutic effects aimed at preserving or restoring neuronal network integrity and contribute to better-informed intervention choices in future clinical trials in AD.

Indexed as

Models, NeurologicalAlzheimer DiseaseBrainComputational BiologyConnectomeHumansNerve NetNeurons

Identifiers

PMID28938009
PMCPMC5627940
OpenAlexW2759472391

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.