ArticleMolecular neurodegeneration2017
Abnormal dendritic calcium activity and synaptic depotentiation occur early in a mouse model of Alzheimer's disease.
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 56 citations in OpenAlex.
- Parvalbumin interneurons in Alzheimer's disease: Physiological insights and pathophysiological mechanisms.Journal of cell communication and signaling · 2026Review
- Targeting PTGS2/NF-κB Pathway: MG-132's Role in Reducing Ischemic Stroke Injury.Biochemical genetics · 2026Article
- Astrocyte Proximity Protects Synapses From Human Amyloid-Beta Induced Degeneration in a Mouse Ex Vivo Model of Early Alzheimer's Disease.The European journal of neuroscience · 2026Article
- Dissecting neuronal circuit function and dysfunction in Alzheimer's disease mouse models: from conventional calcium imaging analysis to machine learning-based approaches.Frontiers in aging neuroscience · 2026Review
- Clearing truncated tau protein restores neuronal function and prevents microglia activation in tauopathy mice.Cell reports · 2025Article
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Cell-specific Nav1.6 knockdown reduced astrocyte-derived Aβ by reverse NaJournal of advanced research · 2025Article
- The Dose-Dependent Effects of Fluorocitrate on the Metabolism and Activity of Astrocytes and Neurons.Brain sciences · 2025Article
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- Ex vivo propagation of synaptically-evoked cortical depolarizations in a mouse model of Alzheimer's disease at 20 Hz, 40 Hz, or 83 Hz.Scientific reports · 2024Article
- Updated Toolbox for Assessing Neuronal Network Reconstruction after Cell Therapy.Bioengineering (Basel, Switzerland) · 2024Review
- Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer's pathology.Nature communications · 2024Article
- Insights on the Use of Transgenic Mice Models in Alzheimer's Disease Research.International journal of molecular sciences · 2024Review
- Anti-Hebbian plasticity in the motor cortex promotes defensive freezing.Current biology : CB · 2023Article
- Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex.Biomedicines · 2022Review
- Biophysical KeLife · 2022Article
- CaMKIIα Signaling Is Required for the Neuroprotective Effects of Dl-3-n-Butylphthalide in Alzheimer's Disease.Molecular neurobiology · 2022Article
- Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis.International journal of molecular sciences · 2022Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAlzheimer's disease (AD) is characterized by amyloid deposition, tangle formation as well as synapse loss. Synaptic abnormalities occur early in the pathogenesis of AD. Identifying early synaptic abnormalities and their underlying mechanisms is likely important for the prevention and treatment of AD.
methodsWe performed in vivo two-photon calcium imaging to examine the activities of somas, dendrites and dendritic spines of layer 2/3 pyramidal neurons in the primary motor cortex in the APPswe/PS1dE9 mouse model of AD and age-matched wild type control mice. We also performed calcium imaging to determine the effect of Aβ oligomers on dendritic calcium activity. In addition, structural and functional two-photon imaging were used to examine the link between abnormal dendritic calcium activity and changes in dendritic spine size in the AD mouse model.
resultsWe found that somatic calcium activities of layer 2/3 neurons were significantly lower in the primary motor cortex of 3-month-old APPswe/PS1dE9 mice than in wild type mice during quiet resting, but not during running on a treadmill. Notably, a significantly larger fraction of apical dendrites of layer 2/3 pyramidal neurons showed calcium transients with abnormally long duration and high peak amplitudes during treadmill running in AD mice. Administration of Aβ oligomers into the brain of wild type mice also induced abnormal dendritic calcium transients during running. Furthermore, we found that the activity and size of dendritic spines were significantly reduced on dendritic branches with abnormally prolonged dendritic calcium transients in AD mice.
conclusionOur findings show that abnormal dendritic calcium transients and synaptic depotentiation occur before amyloid plaque formation in the motor cortex of the APPswe/PS1dE9 mouse model of AD. Dendritic calcium transients with abnormally long durations and high amplitudes could be induced by soluble Aβ oligomers and contribute to synaptic deficits in the early pathogenesis of AD.
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