ArticleScience (New York, N.Y.)2019
A vicious cycle of β amyloid-dependent neuronal hyperactivation.
Article in Science (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 365 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
365 citing papers in PubMed, 3 syntheses or guidelines pooled it, 641 citations in OpenAlex.
- Task-based fMRI brain activation in mild cognitive impairment and Alzheimer's disease: an ALE meta-analysis.GeroScience · 2026Pooled it
- Association between FDG- and TSPO-PET signals across human and animal studies investigating neurodegenerative conditions: a systematic review.Molecular psychiatry · 2026Pooled it
- Decreased Brain pH Correlated With Progression of Alzheimer Disease Neuropathology: A Systematic Review and Meta-Analyses of Postmortem Studies.The international journal of neuropsychopharmacology · 2024Pooled it
- Safety, tolerability and immunogenicity of vaccine ALZ-101 in patients with early Alzheimer's disease: randomised, controlled trial.Alzheimer's research & therapy · 2026Trial
- Input-output curves demonstrate motor cortex hyperexcitability associated with cognitive impairment in Alzheimer's disease.Neurobiology of aging · 2026Article
- Characterizing hippocampal activation during pattern separation with multi-echo fMRI in cognitively normal older adults.Brain imaging and behavior · 2026Article
- Intranasal Artesunate Ameliorates Hippocampal LFP Abnormalities and Cellular Apoptosis in APP/PS1 Mice via a Mechanism Involving GHRH/PI3K/AKT Signaling.Molecular neurobiology · 2026Article
- Multi-functional bionic nanoparticles for precise neuronal targeting and synergistic therapy in Alzheimer's disease.Materials today. Bio · 2026Article
- mTORC1 Activation Links Chronic Stress to Meso-Circuit Desynchronization and Accelerated Amyloid Pathology via Autophagic Dysfunction.CNS neuroscience & therapeutics · 2026Article
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- Review
- Alzheimer's disease through the lens of mesenchymal drift: the collapse of cellular identity.BMB reports · 2026Review
- 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
- Riluzole shifts glial responses to protect synapses and memory in Aβ oligomer-treated rats.Journal of neuroinflammation · 2026Article
- Entorhinal Astrocyte Transplants Restore Spatial Exploration and Alleviate Amyloid-Beta Pathology in Alzheimer's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting soluble misfolded oligomers in anti-amyloid research.Nature reviews. Chemistry · 2026Review
- Neuromodulatory roles of the sigma-1 receptor in behavior and drug sensitization during development.Acta pharmacologica Sinica · 2026Article
- State-Dependent Alterations of Hippocampal Theta-Gamma Coupling in 5xFAD Mice and Their Differential Modulation by Donepezil.Brain sciences · 2026Article
- Medial entorhinal-hippocampal desynchronization parallels the emergence of memory impairment in a mouse model of Alzheimer's disease pathology.Cell reports · 2026Article
- Dopamine Compensates for Amyloid-Induced Default Mode Network Dysfunction to Support Learning.bioRxiv : the preprint server for biology · 2026Article
305 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
β-amyloid (Aβ)-dependent neuronal hyperactivity is believed to contribute to the circuit dysfunction that characterizes the early stages of Alzheimer's disease (AD). Although experimental evidence in support of this hypothesis continues to accrue, the underlying pathological mechanisms are not well understood. In this experiment, we used mouse models of Aβ-amyloidosis to show that hyperactivation is initiated by the suppression of glutamate reuptake. Hyperactivity occurred in neurons with preexisting baseline activity, whereas inactive neurons were generally resistant to Aβ-mediated hyperactivation. Aβ-containing AD brain extracts and purified Aβ dimers were able to sustain this vicious cycle. Our findings suggest a cellular mechanism of Aβ-dependent neuronal dysfunction that can be active before plaque formation.
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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.