ArticleScience advances2025
Neurophysiological signatures of default mode network dysfunction and cognitive decline in Alzheimer's disease.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03875638 (Treating Hyperexcitability in Alzheimer's Disease With Levetiracetam to Improve Brain Function and Cognition), which is not on this map. Cited by 2 papers.
What it found
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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.
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.
Treating Hyperexcitability in Alzheimer's Disease With Levetiracetam to Improve Brain Function and Cognition
Who cites it
2 citing papers in PubMed.
- Clinical utility and prospective of TMS-EEG: Updated review from an international expert group.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2026Review
- The Role of Transcranial Magnetic Stimulation for the Treatment of Alzheimer's Disease: A Narrative Review.Life (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Neural hyperexcitability and network dysfunction are neurophysiological hallmarks of Alzheimer's disease (AD) in animal studies, but their presence and clinical relevance in humans remain poorly understood. We introduce a perturbation-based approach combining transcranial magnetic stimulation and electroencephalography (TMS-EEG), alongside resting-state EEG (rsEEG), to investigate neurophysiological basis of default mode network (DMN) dysfunction in early AD. While rsEEG revealed global neural slowing and disrupted synchrony, these measures reflected widespread changes in brain neurophysiology without network-specific insights. In contrast, TMS-EEG identified network-specific local hyperexcitability in the parietal DMN and disrupted connectivity with frontal DMN regions, which uniquely predicted distinct cognitive impairments and mediated the link between structural brain integrity and cognition. Our findings provide critical insights into how network-specific neurophysiological disruptions contribute to AD-related cognitive dysfunction. Perturbation-based assessments hold promise as potential markers of early detection, disease progression, and target engagement for disease-modifying therapies aiming to restore abnormal neurophysiology in AD.
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Registered trials
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 Socratic graph.