ArticleCerebral cortex (New York, N.Y. : 1991)2020
Hyperexcitability in Aging Is Lost in Alzheimer's: What Is All the Excitement About?
Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The rise and deceleration of neuronal excitability in aging and Alzheimer's disease: Mechanisms, implications, and therapeutic targets.Ageing research reviews · 2026Review
- Behavioral deficits and exacerbated neural and hemodynamic odor responses during lifespan of a mouse model of late onset Alzheimer's disease expressing humanized APOEε4 and Trem2*R47H.Frontiers in aging neuroscience · 2026Article
- Axonal energy metabolism, and the effects in aging and neurodegenerative diseases.Molecular neurodegeneration · 2023Review
- Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease.Frontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal hyperexcitability has emerged as a potential biomarker of late-onset early-stage Alzheimer's disease (LEAD). We hypothesize that the aging-related posterior cortical hyperexcitability anticipates the loss of excitability with the emergence of impairment in LEAD. To test this hypothesis, we compared the behavioral and neurophysiological responses of young and older (ON) normal adults, and LEAD patients during a visuospatial attentional control task. ONs show frontal cortical signal incoherence and posterior cortical hyper-responsiveness with preserved attentional control. LEADs lose the posterior hyper-responsiveness and fail in the attentional task. Our findings suggest that signal incoherence and cortical hyper-responsiveness in aging may contribute to the development of functional impairment in LEAD.
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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 OpenQuestion graph.