ArticleDisease models & mechanisms2019
Amyotrophic lateral sclerosis mutant TDP-43 may cause synaptic dysfunction through altered dendritic spine function.
Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 56 citations in OpenAlex.
- Multiple motor proteins regulate TDP-43 anterograde axonal transport.Acta neuropathologica · 2026Article
- Dietary modulation of the gut microbiome as a supportive strategy in the treatment of amyotrophic lateral sclerosis - a narrative review.Pharmacological reports : PR · 2025Review
- Network Dysfunction Precedes Neurodegeneration in a dox-Regulatable TDP-43 Mouse Model of ALS-FTD.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Review
- Review
- PKCε inhibition prevents ischemia‑induced dendritic spine impairment in cultured primary neurons.Experimental and therapeutic medicine · 2023Article
- Synaptic expression of TAR-DNA-binding protein 43 in the mouse spinal cord determined using super-resolution microscopy.Frontiers in molecular neuroscience · 2023Article
- Familial ALS-associatedOpen biology · 2022Article
- Modulation of synaptic plasticity, motor unit physiology, and TDP-43 pathology by CHCHD10.Acta neuropathologica communications · 2022Article
- Selective vulnerability of tripartite synapses in amyotrophic lateral sclerosis.Acta neuropathologica · 2022Article
- Mitochondrial dysregulation occurs early in ALS motor cortex with TDP-43 pathology and suggests maintaining NADScientific reports · 2022Article
- Synaptic dysfunction in ALS and FTD: anatomical and molecular changes provide insights into mechanisms of disease.Frontiers in molecular neuroscience · 2022Review
- Molecular Pathways Involved in Frontotemporal Lobar Degeneration with TDP-43 Proteinopathy: What Can We Learn from Proteomics?International journal of molecular sciences · 2021Review
- Differential NPY-Y1 Receptor Density in the Motor Cortex of ALS Patients and Familial Model of ALS.Brain sciences · 2021Article
- Cytoplasmic Human TDP-43 Mislocalization Induces Widespread Dendritic Spine Loss in Mouse Upper Motor Neurons.Brain sciences · 2021Article
- Synaptic dysfunction in amyotrophic lateral sclerosis/frontotemporal dementia: Therapeutic strategies and novel biomarkers.Journal of neuroscience research · 2021Review
- Molecular Mechanisms Underlying TDP-43 Pathology in Cellular and Animal Models of ALS and FTLD.International journal of molecular sciences · 2021Review
- Functional Genomics of Axons and Synapses to Understand Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Review
- TDP-43 mediated blood-brain barrier permeability and leukocyte infiltration promote neurodegeneration in a low-grade systemic inflammation mouse model.Journal of neuroinflammation · 2020Article
- CHCHD10-regulated OPA1-mitofilin complex mediates TDP-43-induced mitochondrial phenotypes associated with frontotemporal dementia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Altered cortical excitability and synapse dysfunction are early pathogenic events in amyotrophic lateral sclerosis (ALS) patients and animal models. Recent studies propose an important role for TAR DNA-binding protein 43 (TDP-43), the mislocalization and aggregation of which are key pathological features of ALS. However, the relationship between ALS-linked TDP-43 mutations, excitability and synaptic function is not fully understood. Here, we investigate the role of ALS-linked mutant TDP-43 in synapse formation by examining the morphological, immunocytochemical and excitability profile of transgenic mouse primary cortical pyramidal neurons that over-express human TDP-43
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