ArticleNeurogenetics2012
Axonal transport deficit in a KIF5A( -/- ) mouse model.
Article in Neurogenetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Effect of ALA on preventing diabetic peripheral neuropathy in rats through mitochondrial axonal transport.PloS one · 2026Article
- Role of LRRK2 in axonal transport and Parkinson's disease.The Biochemical journal · 2025Review
- One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.Cell communication and signaling : CCS · 2025Review
- A novel antidepressant mechanism of baicalin: enhancing KIF5A-mediated axoplasmic transport and vesicular trafficking in glutamatergic neurons.Frontiers in pharmacology · 2025Article
- Altered molecular and cellular mechanisms in KIF5A-associated neurodegenerative or neurodevelopmental disorders.Cell death & disease · 2024Article
- KIF5A regulates axonal repair and time-dependent axonal transport of SFPQ granules and mitochondria in human motor neurons.bioRxiv : the preprint server for biology · 2024Article
- ALS-associated C21ORF2 variant disrupts DNA damage repair, mitochondrial metabolism, neuronal excitability and NEK1 levels in human motor neurons.Acta neuropathologica communications · 2024Article
- The ALS-associated KIF5A P986L variant is not pathogenic for Drosophila motoneurons.Scientific reports · 2024Article
- Static magnetic field-modulated mesenchymal stem cell-derived mitochondria-containing microvesicles for enhanced intervertebral disc degeneration therapy.Journal of nanobiotechnology · 2024Article
- 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
- Role of microtubule actin crosslinking factor 1 (MACF1) in bipolar disorder pathophysiology and potential in lithium therapeutic mechanism.Translational psychiatry · 2023Review
- Impaired motor unit recovery and maintenance in a knock-in mouse model of ALS-associated Kif5a variant.Neurobiology of disease · 2023Article
- Kif5a Regulates Mitochondrial Transport in Developing Retinal Ganglion Cells In Vitro.Investigative ophthalmology & visual science · 2023Article
- Dysregulated expression and distribution of Kif5α in neurites of wobbler motor neurons.Neural regeneration research · 2023Article
- Mitochondrial transport in neurons and evidence for its involvement in acute neurological disorders.Frontiers in neuroscience · 2023Review
- Axonal transport deficits in the pathogenesis of diabetic peripheral neuropathy.Frontiers in endocrinology · 2023Review
- Heroin Addiction Induces Axonal Transport Dysfunction in the Brain Detected by In Vivo MRI.Neurotoxicity research · 2022Article
- Axon Biology in ALS: Mechanisms of Axon Degeneration and Prospects for Therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Tau phosphorylation and PAD exposure in regulation of axonal growth.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Hereditary spastic paraplegia (HSP) is a neurodegenerative disorder preferentially affecting the longest corticospinal axons. More than 40 HSP genetic loci have been identified, among them SPG10, an autosomal dominant HSP caused by point mutations in the neuronal kinesin heavy chain protein KIF5A. Constitutive KIF5A knockout (KIF5A( -/- )) mice die early after birth. In these mice, lungs were unexpanded, and cell bodies of lower motor neurons in the spinal cord swollen, but the pathomechanism remained unclear. To gain insights into the pathophysiology, we characterized survival, outgrowth, and function in primary motor and sensory neuron cultures from KIF5A( -/- ) mice. Absence of KIF5A reduced survival in motor neurons, but not in sensory neurons. Outgrowth of axons and dendrites was remarkably diminished in KIF5A( -/- ) motor neurons. The number of axonal branches was reduced, whereas the number of dendrites was not altered. In KIF5A( -/- ) sensory neurons, neurite outgrowth was decreased but the number of neurites remained unchanged. In motor neurons maximum and average velocity of mitochondrial transport was reduced both in anterograde and retrograde direction. Our results point out a role of KIF5A in process outgrowth and axonal transport of mitochondria, affecting motor neurons more severely than sensory neurons. This gives pathophysiological insights into KIF5A associated HSP, and matches the clinical findings of predominant degeneration of the longest axons of the corticospinal tract.
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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.