ReviewJournal of Alzheimer's disease : JAD2022
Functional Neurophysiological Biomarkers of Early-Stage Alzheimer's Disease: A Perspective of Network Hyperexcitability in Disease Progression.
Review in Journal of Alzheimer's disease : JAD, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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.
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.
Who cites it
27 citing papers in PubMed.
- Input-output curves demonstrate motor cortex hyperexcitability associated with cognitive impairment in Alzheimer's disease.Neurobiology of aging · 2026Article
- Diurnal dynamics of multilayer brain networks predict cognitive trajectories in aging.GeroScience · 2026Article
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- Sleep Deprivation and Neuronal Hyperexcitation Share Transcriptomic Signatures.Neuropsychopharmacology reports · 2026Article
- Distinct Transcriptional States of TDP-43 Pathology in an Alzheimer's Disease Mouse Model.Neuroscience bulletin · 2026Article
- Alterations in topological and dynamical parameters correlate with disease biomarkers and neuropsychological scores in prodromic stages of dementia.Scientific reports · 2026Article
- Article
- Early aperiodic EEG changes in preclinical and prodromal Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Astrocytic KFrontiers in aging neuroscience · 2026Review
- Tau pathology reprograms glucose metabolism to support cortical hyperexcitability, excitatory/inhibitory imbalance, and sleep loss.NPJ dementia · 2026Article
- Advances in AI-based diagnosis of Alzheimer's disease using MRI: a comprehensive survey.Frontiers in medicine · 2026Review
- Insulin signaling disruption exacerbates memory impairment and seizure susceptibility in an epilepsy model with Alzheimer's disease-like pathology.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Hyperactive neuronal networks enhance tau spread in an Alzheimer's disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Cerebellar Contributions to Hypokinetic Symptoms in an Acute Lesion Parkinsonism Model.Neurology international · 2025Article
- Hippocampal and cortical activities reflect early hyperexcitability in an Alzheimer's mouse model.Brain communications · 2025Article
- Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Network Hyperexcitability in Early-Stage Alzheimer's Disease: Evaluation of Functional Connectivity Biomarkers in a Computational Disease Model.Journal of Alzheimer's disease : JAD · 2024Article
- Olfactory deficits in aging and Alzheimer's-spotlight on inhibitory interneurons.Frontiers in neuroscience · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Network hyperexcitability (NH) has recently been suggested as a potential neurophysiological indicator of Alzheimer's disease (AD), as new, more accurate biomarkers of AD are sought. NH has generated interest as a potential indicator of certain stages in the disease trajectory and even as a disease mechanism by which network dysfunction could be modulated. NH has been demonstrated in several animal models of AD pathology and multiple lines of evidence point to the existence of NH in patients with AD, strongly supporting the physiological and clinical relevance of this readout. Several hypotheses have been put forward to explain the prevalence of NH in animal models through neurophysiological, biochemical, and imaging techniques. However, some of these hypotheses have been built on animal models with limitations and caveats that may have derived NH through other mechanisms or mechanisms without translational validity to sporadic AD patients, potentially leading to an erroneous conclusion of the underlying cause of NH occurring in patients with AD. In this review, we discuss the substantiation for NH in animal models of AD pathology and in human patients, as well as some of the hypotheses considering recently developed animal models that challenge existing hypotheses and mechanisms of NH. In addition, we provide a preclinical perspective on how the development of animal models incorporating AD-specific NH could provide physiologically relevant translational experimental data that may potentially aid the discovery and development of novel therapies for AD.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.