ArticleCell reports2022
Disrupted neural correlates of anesthesia and sleep reveal early circuit dysfunctions in Alzheimer models.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- The default mode network exhibits circuit-specific selective vulnerability despite widespread amyloid burden in an animal model of Alzheimer's disease.Nature communications · 2026Article
- Reduced inhibition, bursting, and accelerated oscillations drive early hippocampal hyperactivity in Alzheimer's disease in vivo.Communications biology · 2026Article
- Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.Nature communications · 2026Article
- Wakefulness regulation of memory encoding and retrieval: structure and activity.National science review · 2026Review
- Sleep firing rate homeostasis is disrupted in mild parkinsonism.NPJ Parkinson's disease · 2026Article
- Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of alzheimer's disease.Scientific reports · 2025Article
- Partial normalization of hippocampal oscillatory activity during sleep in TgF344-AD rats coincides with increased cholinergic synapses at early-plaque stage of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Impaired hippocampal circuit function underlying memory encoding and consolidation precede robust Aβ deposition in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- LOU/c/jall rat as a model of resilience in the context of streptozotocin-induced cognitive impairment.Frontiers in aging neuroscience · 2025Article
- Early hippocampal hyperexcitability and synaptic reorganization in mouse models of amyloidosis.iScience · 2024Article
- β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer's Disease.Nature communications · 2024Article
- The selfish network: how the brain preserves behavioral function through shifts in neuronal network state.Trends in neurosciences · 2024Review
- Linking activity dyshomeostasis and sleep disturbances in Alzheimer disease.Nature reviews. Neuroscience · 2024Review
- Deep brain stimulation of thalamic nucleus reuniens promotes neuronal and cognitive resilience in an Alzheimer's disease mouse model.Nature communications · 2023Article
- Electric Field Effects on Brain Activity: Implications for Epilepsy and Burst Suppression.Cells · 2023Article
- Logarithmically scaled, gamma distributed neuronal spiking.The Journal of physiology · 2023Review
- Early alterations in the MCH system link aberrant neuronal activity and sleep disturbances in a mouse model of Alzheimer's disease.Nature neuroscience · 2023Article
- Disruption of hippocampal neuronal circuit function depends upon behavioral state in the APP/PS1 mouse model of Alzheimer's disease.Scientific reports · 2022Article
- A Comparison of Brain-State Dynamics across Common Anesthetic Agents in Male Sprague-Dawley Rats.International journal of molecular sciences · 2022Article
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated homeostasis of neural activity has been hypothesized to drive Alzheimer's disease (AD) pathogenesis. AD begins with a decades-long presymptomatic phase, but whether homeostatic mechanisms already begin failing during this silent phase is unknown. We show that before the onset of memory decline and sleep disturbances, familial AD (fAD) model mice display no deficits in CA1 mean firing rate (MFR) during active wakefulness. However, homeostatic down-regulation of CA1 MFR is disrupted during non-rapid eye movement (NREM) sleep and general anesthesia in fAD mouse models. The resultant hyperexcitability is attenuated by the mitochondrial dihydroorotate dehydrogenase (DHODH) enzyme inhibitor, which tunes MFR toward lower set-point values. Ex vivo fAD mutations impair downward MFR homeostasis, resulting in pathological MFR set points in response to anesthetic drug and inhibition blockade. Thus, firing rate dyshomeostasis of hippocampal circuits is masked during active wakefulness but surfaces during low-arousal brain states, representing an early failure of the silent disease stage.
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