ReviewFrontiers in neuroanatomy2014
Retrograde labeling, transduction, and genetic targeting allow cellular analysis of corticospinal motor neurons: implications in health and disease.
Review in Frontiers in neuroanatomy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- High-density multielectrode arrays bring cellular resolution to neuronal activity and network analyses of corticospinal motor neurons.Scientific reports · 2025Article
- Spatiotemporal profile of an optimal host response to virus infection in the primate central nervous system.PLoS pathogens · 2025Article
- Altered Thalamocortical Signaling in a Mouse Model of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Novel rAAV vector mediated intrathecal HGF delivery has an impact on neuroimmune modulation in the ALS motor cortex with TDP-43 pathology.Gene therapy · 2023Article
- 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
- Article
- Advances in Gene Delivery Methods to Label and Modulate Activity of Upper Motor Neurons: Implications for Amyotrophic Lateral Sclerosis.Brain sciences · 2021Review
- Mutations and Protein Interaction Landscape Reveal Key Cellular Events Perturbed in Upper Motor Neurons with HSP and PLS.Brain sciences · 2021Article
- Improving mitochondria and ER stability helps eliminate upper motor neuron degeneration that occurs due to mSOD1 toxicity and TDP-43 pathology.Clinical and translational medicine · 2021Article
- How Degeneration of Cells Surrounding Motoneurons Contributes to Amyotrophic Lateral Sclerosis.Cells · 2020Review
- Assessing neuraxial microstructural changes in a transgenic mouse model of early stage Amyotrophic Lateral Sclerosis by ultra-high field MRI and diffusion tensor metrics.Animal models and experimental medicine · 2020Article
- Article
- The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS.Frontiers in molecular neuroscience · 2020Article
- Complexity of Generating Mouse Models to Study the Upper Motor Neurons: Let Us Shift Focus from Mice to Neurons.International journal of molecular sciences · 2019Review
- Pathophysiology and Diagnosis of ALS: Insights from Advances in Neurophysiological Techniques.International journal of molecular sciences · 2019Review
- Mitochondria, ER, and nuclear membrane defects reveal early mechanisms for upper motor neuron vulnerability with respect to TDP-43 pathology.Acta neuropathologica · 2019Article
- Evidence for an early innate immune response in the motor cortex of ALS.Journal of neuroinflammation · 2017Article
- Calretinin and Neuropeptide Y interneurons are differentially altered in the motor cortex of the SOD1Scientific reports · 2017Article
- Cortical synaptic and dendritic spine abnormalities in a presymptomatic TDP-43 model of amyotrophic lateral sclerosis.Scientific reports · 2016Article
- Pathophysiological and diagnostic implications of cortical dysfunction in ALS.Nature reviews. Neurology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Corticospinal motor neurons (CSMN) have a unique ability to receive, integrate, translate, and transmit the cerebral cortex's input toward spinal cord targets and therefore act as a "spokesperson" for the initiation and modulation of voluntary movements that require cortical input. CSMN degeneration has an immense impact on motor neuron circuitry and is one of the underlying causes of numerous neurodegenerative diseases, such as primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), and amyotrophic lateral sclerosis (ALS). In addition, CSMN death results in long-term paralysis in spinal cord injury patients. Detailed cellular analyses are crucial to gain a better understanding of the pathologies underlying CSMN degeneration. However, visualizing and identifying these vulnerable neuron populations in the complex and heterogeneous environment of the cerebral cortex have proved challenging. Here, we will review recent developments and current applications of novel strategies that reveal the cellular and molecular basis of CSMN health and vulnerability. Such studies hold promise for building long-term effective treatment solutions in the near future.
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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.