ArticleNature communications2023
Deep brain stimulation of thalamic nucleus reuniens promotes neuronal and cognitive resilience in an Alzheimer's disease mouse model.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Neuromodulation techniques targeting neurotransmitter dysfunction: Innovation in treatments for Alzheimer's disease.Neural regeneration research · 2026Article
- The mPFC-reuniens-hippocampus pathway links brain circuitry and neural plasticity in antidepressant response.Nature communications · 2026Article
- Large-Scale Neural Recording Technologies for Investigating Circuit Dysfunction and Functional Biomarker Discovery in Animal Models of Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Stable neuronal representations underlie cognitive resilience to Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Beyond seizure control: Identifying deficits in cognitive networks in absence epilepsy.Science advances · 2026Article
- Implication of the thalamus in sleep alterations observed in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- The thalamic nucleus reuniens orchestrates prefrontal-hippocampal synchrony in memory, emotion, and disease.Frontiers in behavioral neuroscience · 2026Review
- Stable neuronal representations to repeated stimulation underlie cognitive resilience in Alzheimer's disease pathology.bioRxiv : the preprint server for biology · 2025Article
- Thalamo-hippocampal pathway determines aggression and self-harm.Science advances · 2025Article
- State-dependent memory mechanisms insights from neural circuits and clinical implications.Frontiers in cellular neuroscience · 2025Review
- Calcium Signalling in Neurological Disorders, with Insights from Miniature Fluorescence Microscopy.Cells · 2024Review
- Early hippocampal hyperexcitability and synaptic reorganization in mouse models of amyloidosis.iScience · 2024Article
- Article
- Choline supplementation in early life improves and low levels of choline can impair outcomes in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Linking activity dyshomeostasis and sleep disturbances in Alzheimer disease.Nature reviews. Neuroscience · 2024Review
- The selfish network: how the brain preserves behavioral function through shifts in neuronal network state.Trends in neurosciences · 2024Review
- "Back to Braak": Role of Nucleus Reuniens and Subcortical Pathways in Alzheimer's Disease Progression.The journal of prevention of Alzheimer's disease · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms that confer cognitive resilience to Alzheimer's Disease (AD) are not fully understood. Here, we describe a neural circuit mechanism underlying this resilience in a familial AD mouse model. In the prodromal disease stage, interictal epileptiform spikes (IESs) emerge during anesthesia in the CA1 and mPFC regions, leading to working memory disruptions. These IESs are driven by inputs from the thalamic nucleus reuniens (nRE). Indeed, tonic deep brain stimulation of the nRE (tDBS-nRE) effectively suppresses IESs and restores firing rate homeostasis under anesthesia, preventing further impairments in nRE-CA1 synaptic facilitation and working memory. Notably, applying tDBS-nRE during the prodromal phase in young APP/PS1 mice mitigates age-dependent memory decline. The IES rate during anesthesia in young APP/PS1 mice correlates with later working memory impairments. These findings highlight the nRE as a central hub of functional resilience and underscore the clinical promise of DBS in conferring resilience to AD pathology by restoring circuit-level homeostasis.
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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.