ArticleFrontiers in aging neuroscience2021
Analysis of Age-Dependent Alterations in Excitability Properties of CA1 Pyramidal Neurons in an APPPS1 Model of Alzheimer's Disease.
Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 24 citations in OpenAlex.
- Prodromal changes in cortical neuron physiology before amyloid pathology in a mild model of Alzheimer's disease.Scientific reports · 2026Article
- Reduced inhibition, bursting, and accelerated oscillations drive early hippocampal hyperactivity in Alzheimer's disease in vivo.Communications biology · 2026Article
- Transcriptomic alterations in APP/PS1 mice astrocytes lead to early postnatal axon initial segment structural changes.Cellular and molecular life sciences : CMLS · 2024Article
- Early hippocampal hyperexcitability and synaptic reorganization in mouse models of amyloidosis.iScience · 2024Article
- Article
- Alzheimer's disease induced neurons bearingFrontiers in cellular neuroscience · 2024Article
- Immune senescence in aged APP/PS1 mice.NeuroImmune pharmacology and therapeutics · 2023Article
- Review
- Different responses of mice and rats hippocampus CA1 pyramidal neurons toFrontiers in cellular neuroscience · 2023Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- Selective Menin Deletion in the Hippocampal CA1 Region Leads to Disruption of Contextual Memory in theCells · 2022Article
- Altered membrane properties but unchanged intrinsic excitability and spontaneous postsynaptic currents in an aged APPFrontiers in cellular neuroscience · 2022Article
- The EBRAINS Hodgkin-Huxley Neuron Builder: An online resource for building data-driven neuron models.Frontiers in neuroinformatics · 2022Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-dependent accumulation of amyloid-β, provoking increasing brain amyloidopathy, triggers abnormal patterns of neuron activity and circuit synchronization in Alzheimer's disease (AD) as observed in human AD patients and AD mouse models. Recent studies on AD mouse models, mimicking this age-dependent amyloidopathy, identified alterations in CA1 neuron excitability. However, these models generally also overexpress mutated amyloid precursor protein (APP) and presenilin 1 (PS1) and there is a lack of a clear correlation of neuronal excitability alterations with progressive amyloidopathy. The active development of computational models of AD points out the need of collecting such experimental data to build a reliable disease model exhibiting AD-like disease progression. We therefore used the feature extraction tool of the Human Brain Project (HBP) Brain Simulation Platform to systematically analyze the excitability profile of CA1 pyramidal neuron in the APPPS1 mouse model. We identified specific features of neuron excitability that best correlate either with over-expression of mutated APP and PS1 or increasing Aβ amyloidopathy. Notably, we report strong alterations in membrane time constant and action potential width and weak alterations in firing behavior. Also, using a CA1 pyramidal neuron model, we evidence amyloidopathy-dependent alterations in
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