ArticleAlzheimer's research & therapy2022
A multiscale brain network model links Alzheimer's disease-mediated neuronal hyperactivity to large-scale oscillatory slowing.
Article in Alzheimer's research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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53 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Tracking electrophysiological signatures of Alzheimer's disease: a systematic review of multimodal studies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Pooled it
- Connectome-Guided Personalization of Optimal TDCS Intervention Selection in Alzheimer's Disease: A Modeling Study.eNeuro · 2026Article
- Alterations in topological and dynamical parameters correlate with disease biomarkers and neuropsychological scores in prodromic stages of dementia.Scientific reports · 2026Article
- Individual cases of Parkinson's disease can be robustly classified using magnetoencephalography.NPJ Parkinson's disease · 2026Article
- Correspondence of Basal Forebrain Resting-State Functional Connectivity and Cerebral Glucose Metabolism Alterations With Neurotransmitter Maps in Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Article
- A Framework Integrating Spiking Cortical Circuit Modeling and Simulation-Based Inference to Probe Biomarkers of Cortical Dysfunction in Alzheimer's Disease.Interdisciplinary sciences, computational life sciences · 2026Article
- 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 · 2026Review
- Digital twins support cross-modal and cross-centric classification of mild cognitive impairment.Communications medicine · 2026Article
- Fast Interneuron Dysfunction in Laminar Neural Mass Model Reproduces Alzheimer's Oscillatory Biomarkers.Human brain mapping · 2026Article
- EEG-based detection of early functional brain changes in subjective cognitive decline: a prospective cohort study.Alzheimer's research & therapy · 2025Article
- Stable individualized brain computing model informed by spatiotemporal co-activity patterns.PLoS computational biology · 2025Article
- Acrolein-Induced Alterations in Morphology and Stress Resilience in hiPSC-Derived Cortical Neurons.Environmental science & technology · 2025Article
- Molecular and neuropathological determinants of neuronal dysfunction in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Digital twins and non-invasive recordings enable early diagnosis of Alzheimer's disease.Alzheimer's research & therapy · 2025Observational
- Exploring the neuromagnetic signatures of cognitive decline from mild cognitive impairment to Alzheimer's disease dementia.EBioMedicine · 2025Article
- Longitudinal excitation-inhibition balance altered by sex and APOE-ε4.Communications biology · 2025Article
- The Bidirectional Relationship Between Epilepsy and Alzheimer's Disease.Current neurology and neuroscience reports · 2025Review
- An Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.Molecular neurobiology · 2025Review
- Revealing excitation-inhibition imbalance in Alzheimer's disease using multiscale neural model inversion of resting-state functional MRI.Communications medicine · 2025Article
- Brain Segregation and Integration Relate to Word-Finding Abilities in Older and Younger Adults.Neurobiology of language (Cambridge, Mass.) · 2025Article
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6 authors at 1 institution in 1 country.
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Abstract
backgroundNeuronal hyperexcitability and inhibitory interneuron dysfunction are frequently observed in preclinical animal models of Alzheimer's disease (AD). This study investigates whether these microscale abnormalities explain characteristic large-scale magnetoencephalography (MEG) activity in human early-stage AD patients.
methodsTo simulate spontaneous electrophysiological activity, we used a whole-brain computational network model comprised of 78 neural masses coupled according to human structural brain topology. We modified relevant model parameters to simulate six literature-based cellular scenarios of AD and compare them to one healthy and six contrast (non-AD-like) scenarios. The parameters include excitability, postsynaptic potentials, and coupling strength of excitatory and inhibitory neuronal populations. Whole-brain spike density and spectral power analyses of the simulated data reveal mechanisms of neuronal hyperactivity that lead to oscillatory changes similar to those observed in MEG data of 18 human prodromal AD patients compared to 18 age-matched subjects with subjective cognitive decline.
resultsAll but one of the AD-like scenarios showed higher spike density levels, and all but one of these scenarios had a lower peak frequency, higher spectral power in slower (theta, 4-8Hz) frequencies, and greater total power. Non-AD-like scenarios showed opposite patterns mainly, including reduced spike density and faster oscillatory activity. Human AD patients showed oscillatory slowing (i.e., higher relative power in the theta band mainly), a trend for lower peak frequency and higher total power compared to controls. Combining model and human data, the findings indicate that neuronal hyperactivity can lead to oscillatory slowing, likely due to hyperexcitation (by hyperexcitability of pyramidal neurons or greater long-range excitatory coupling) and/or disinhibition (by reduced excitability of inhibitory interneurons or weaker local inhibitory coupling strength) in early AD.
conclusionsUsing a computational brain network model, we link findings from different scales and models and support the hypothesis of early-stage neuronal hyperactivity underlying E/I imbalance and whole-brain network dysfunction in prodromal AD.
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