ArticleActa neuropathologica communications2016
Marked changes in dendritic structure and spine density precede significant neuronal death in vulnerable cortical pyramidal neuron populations in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.
Article in Acta neuropathologica communications, 2016. 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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53 citing papers in PubMed, 77 citations in OpenAlex.
- Morphological segmentation with tiling light sheet microscopy to quantitatively analyze the three-dimensional structures of spinal motoneurons.Cell regeneration (London, England) · 2025Article
- Multi-path direct current spinal stimulation extended survival in the SOD1-G93A model of amyotrophic lateral sclerosis.Frontiers in neurology · 2025Article
- Early disruption of the CREB pathway drives dendritic morphological alterations in FTD/ALS cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Dendrite injury triggers neuroprotection in Drosophila models of neurodegenerative disease.Scientific reports · 2024Article
- Prion protein pathology in Ubiquilin 2 models of ALS.Neurobiology of disease · 2024Article
- Sleep Apnea and Amyotrophic Lateral Sclerosis: Cause, Correlation, Any Relation?Brain sciences · 2024Review
- Nicotinamide Adenine Dinucleotide Precursor Supplementation Modulates Neurite Complexity and Survival in Motor Neurons from Amyotrophic Lateral Sclerosis Models.Antioxidants & redox signaling · 2024Article
- Revisiting Glutamate Excitotoxicity in Amyotrophic Lateral Sclerosis and Age-Related Neurodegeneration.International journal of molecular sciences · 2024Review
- How do we get from hyperexcitability to excitotoxicity in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2024Review
- Age-Related Alterations in Gray Matter Microstructure in Older People With Remitted Major Depression at Risk for Dementia.Biological psychiatry global open science · 2024Article
- Dendritic morphology of motor neurons and interneurons within the compact, semicompact, and loose formations of the rat nucleus ambiguus.Frontiers in cellular neuroscience · 2024Article
- Article
- Novel regenerative drug, SPG302 promotes functional recovery of diaphragm muscle activity after cervical spinal cord injury.The Journal of physiology · 2023Article
- The ALS-Related SynGAP1 Pathogenic Variant Causes Dendritic Spine Loss: Potential Mechanisms of Early-Stage ALS Progression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Neuronal models of TDP-43 proteinopathy display reduced axonal translation, increased oxidative stress, and defective exocytosis.Frontiers in cellular neuroscience · 2023Article
- Synaptic remodeling follows upper motor neuron hyperexcitability in a rodent model of TDP-43.Frontiers in cellular neuroscience · 2023Article
- Familial ALS-associatedOpen biology · 2022Article
- Upper motor neurons are a target for gene therapy and UCHL1 is necessary and sufficient to improve cellular integrity of diseased upper motor neurons.Gene therapy · 2022Article
- Mapping Motor Neuron Vulnerability in the Neuraxis of Male SOD1Frontiers in endocrinology · 2022Article
- Muscle-specific deletion of the vitamin D receptor in mice is associated with diaphragm muscle weakness.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
Corrections and comments
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is characterised by the death of upper (corticospinal) and lower motor neurons (MNs) with progressive muscle weakness. This incurable disease is clinically heterogeneous and its aetiology remains unknown. Increased excitability of corticospinal MNs has been observed prior to symptoms in human and rodent studies. Increased excitability has been correlated with structural changes in neuronal dendritic arbors and spines for decades. Here, using a modified Golgi-Cox staining method, we have made the first longitudinal study examining the dendrites of pyramidal neurons from the motor cortex, medial pre-frontal cortex, somatosensory cortex and entorhinal cortex of hSOD1(G93A) (SOD1) mice compared to wild-type (WT) littermate controls at postnatal (P) days 8-15, 28-35, 65-75 and 120. Progressive decreases in dendritic length and spine density commencing at pre-symptomatic ages (P8-15 or P28-35) were observed in layer V pyramidal neurons within the motor cortex and medial pre-frontal cortex of SOD1 mice compared to WT mice. Spine loss without concurrent dendritic pathology was present in the pyramidal neurons of the somatosensory cortex from disease-onset (P65-75). Our results from the SOD1 model suggest that dendritic and dendritic spine changes foreshadow and underpin the neuromotor phenotypes present in ALS and may contribute to the varied cognitive, executive function and extra-motor symptoms commonly seen in ALS patients. Determining if these phenomena are compensatory or maladaptive may help explain differential susceptibility of neurons to degeneration in ALS.
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