ArticleNature communications2025
Distinct manifestations of excitatory-inhibitory imbalance associated with amyloid-β and tau in patients with Alzheimer's disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The Alzheimer's disease risk gene SORL1 is a regulator of excitatory neuronal function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Synaptic vs. Non-Synaptic Glycine Receptors: Physiological Role and Implications in Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- PPT1 selectively depalmitoylates GAP43 to regulate neuronal excitability and cognitive function.Science advances · 2026Article
- Peripheral Mitochondrial Energetics are Associated with Cortical Neurophysiological Alterations in Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2026Article
- Altered rhythmic and arrhythmic electroencephalographic activity during non-rapid eye movement sleep in amnestic mild cognitive impairment.Brain communications · 2026Article
- Multimodal characterization of cortical hyperexcitability as a driver of cognitive decline in neurocognitive disorders: study protocol for the LENDÜLET Neurocognitive Research Project.Frontiers in aging neuroscience · 2026Article
- Microvascular dysfunction and aberrant network activity drive reduced brain oxygenation in a mouse tauopathy model.Research square · 2025Article
- Translating Alzheimer's Disease Mechanisms into Therapeutic Opportunities.Biomolecules · 2025Review
- Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
A growing body of evidence shows that epileptic activity is frequently observed in patients with Alzheimer's disease (AD), implicating underlying excitatory-inhibitory imbalance. The distinction of whether the AD-epileptic phenotype represents a subset of patients or an underdiagnosed manifestation holds major therapeutic implications. Here, we quantified the excitatory-inhibitory imbalance in AD patients using magnetoencephalography and examined the relationships to AD pathophysiology-amyloid-beta and tau, and to epileptic activity. We used two metrics to quantify regional excitatory-inhibitory imbalance distinguishing between local hyperexcitability (Neural excitability, quantified by regional aperiodic spectral slope) and aberrant long-range synaptic input integration (Neural fragility, quantified by regional linear dynamic instability). We found that amyloid-beta correlated with higher neural fragility and higher neural excitability, while tau and hypometabolism uniquely correlated with higher neural excitability. Importantly, the AD-epileptic phenotype showed a distinctive increase in neural fragility. Our findings demonstrate that AD pathophysiology is associated with diverse mechanisms of excitatory-inhibitory imbalance and that AD-epileptic phenotype represents a distinct group of patients with greater impairments in long-range synaptic input integration.
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