ArticleeLife2022
Activity disruption causes degeneration of entorhinal neurons in a mouse model of Alzheimer's circuit dysfunction.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
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Who cites it
12 citing papers in PubMed.
- Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.Science advances · 2026Article
- Structural compression and entorhinal vulnerability: Linking tentorial adjacency to tau burden and dementia progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Structural Compression and Entorhinal Vulnerability: Linking Tentorial Adjacency to Tau Burden and Dementia Progression.bioRxiv : the preprint server for biology · 2025Article
- Neural cell competition sculpting brain from cradle to grave.National science review · 2025Review
- Chemogenetic neuronal silencing decouples c-Jun activation from cell death in the temporal cortex.The European journal of neuroscience · 2024Article
- Astrocytes in selective vulnerability to neurodegenerative disease.Trends in neurosciences · 2024Review
- Article
- Neuronal Vulnerability of the Entorhinal Cortex to Tau Pathology in Alzheimer's Disease.British journal of biomedical science · 2024Review
- Entorhinal cortex-hippocampal circuit connectivity in health and disease.Frontiers in human neuroscience · 2024Review
- Use it or lose it.eLife · 2023Article
- Lower expression ofJournal of Alzheimer's disease reportsArticle
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Authors and funding
9 authors.
Funding
Abstract
Neurodegenerative diseases are characterized by selective vulnerability of distinct cell populations; however, the cause for this specificity remains elusive. Here, we show that entorhinal cortex layer 2 (EC2) neurons are unusually vulnerable to prolonged neuronal inactivity compared with neighboring regions of the temporal lobe, and that reelin + stellate cells connecting EC with the hippocampus are preferentially susceptible within the EC2 population. We demonstrate that neuronal death after silencing can be elicited through multiple independent means of activity inhibition, and that preventing synaptic release, either alone or in combination with electrical shunting, is sufficient to elicit silencing-induced degeneration. Finally, we discovered that degeneration following synaptic silencing is governed by competition between active and inactive cells, which is a circuit refinement process traditionally thought to end early in postnatal life. Our data suggests that the developmental window for wholesale circuit plasticity may extend into adulthood for specific brain regions. We speculate that this sustained potential for remodeling by entorhinal neurons may support lifelong memory but renders them vulnerable to prolonged activity changes in disease.
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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.