ArticleMolecular neurodegeneration2010
A hereditary spastic paraplegia mutation in kinesin-1A/KIF5A disrupts neurofilament transport.
Article in Molecular neurodegeneration, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 80 citations in OpenAlex.
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Targeted plasma proteomics uncover proteins associated with KIF5A-linked SPG10 and ALS spectrum disorders.HGG advances · 2026Article
- Functional validation of the novel KIF5A p.R17Q VUS reveals defective axonal transport in iPSC-motoneurons from a SPG10 patient.Frontiers in genetics · 2026Article
- One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.Cell communication and signaling : CCS · 2025Review
- Neuromuscular dysfunction in patient-derived FUSNAR molecular medicine · 2025Article
- Pluripotent Stem Cells as a Preclinical Cellular Model for Studying Hereditary Spastic Paraplegias.International journal of molecular sciences · 2024Review
- ALS-Associated KIF5A Mutation Causes Locomotor Deficits Associated with Cytoplasmic Inclusions, Alterations of Neuromuscular Junctions, and Motor Neuron Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Impaired motor unit recovery and maintenance in a knock-in mouse model of ALS-associated Kif5a variant.Neurobiology of disease · 2023Article
- The interconnection of endoplasmic reticulum and microtubule and its implication in Hereditary Spastic Paraplegia.Computational and structural biotechnology journal · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Simple models to understand complex disease: 10 years of progress fromFrontiers in neuroscience · 2023Review
- Neurofilaments in health and Charcot-Marie-Tooth disease.Frontiers in cell and developmental biology · 2023Review
- Axonal transport deficits in the pathogenesis of diabetic peripheral neuropathy.Frontiers in endocrinology · 2023Review
- Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease.Frontiers in neuroscience · 2022Article
- Minor Allele Frequencies and Molecular Pathways Differences for SNPs Associated with Amyotrophic Lateral Sclerosis in Subjects Participating in the UKBB and 1000 Genomes Project.Journal of clinical medicine · 2021Article
- Current Knowledge of Endolysosomal and Autophagy Defects in Hereditary Spastic Paraplegia.Cells · 2021Review
- Cytoskeletal regulation guides neuronal trafficking to effectively supply the synapse.Current biology : CB · 2021Review
- Amyotrophic Lateral Sclerosis and Frontotemporal Lobar Degenerations: Similarities in Genetic Background.Diagnostics (Basel, Switzerland) · 2021Review
- A novel strategy to visualize vesicle-bound kinesins reveals the diversity of kinesin-mediated transport.Traffic (Copenhagen, Denmark) · 2019Article
- Altered CSF levels of monoamines in hereditary spastic paraparesis 10: A case series.Neurology. Genetics · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHereditary spastic paraplegias are a group of neurological disorders characterized by progressive distal degeneration of the longest ascending and descending axons in the spinal cord, leading to lower limb spasticity and weakness. One of the dominantly inherited forms of this disease (spastic gait type 10, or SPG10) is caused by point mutations in kinesin-1A (also known as KIF5A), which is thought to be an anterograde motor for neurofilaments.
resultsWe investigated the effect of an SPG10 mutation in kinesin-1A (N256S-kinesin-1A) on neurofilament transport in cultured mouse cortical neurons using live-cell fluorescent imaging. N256S-kinesin-1A decreased both anterograde and retrograde neurofilament transport flux by decreasing the frequency of anterograde and retrograde movements. Anterograde velocity was not affected, whereas retrograde velocity actually increased.
conclusionsThese data reveal subtle complexities to the functional interdependence of the anterograde and retrograde neurofilament motors and they also raise the possibility that anterograde and retrograde neurofilament transport may be disrupted in patients with SPG10.
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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.