ArticleNeurobiology of disease2012
AAV2 mediated retrograde transduction of corticospinal motor neurons reveals initial and selective apical dendrite degeneration in ALS.
Article in Neurobiology of disease, 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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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
53 citing papers in PubMed, 74 citations in OpenAlex.
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- Brain Connectivity, Neural Networks, and Resilience in Aging and Neurodegeneration.The American journal of pathology · 2025Review
- Safety and efficacy evaluation of intracerebroventricular human neural stem cell transplantation in SOD1 mice as a novel approach for ALS.Journal of translational medicine · 2025Article
- The integrity of the corticospinal tract and corpus callosum, and the risk of ALS: univariable and multivariable Mendelian randomization.Scientific reports · 2024Article
- Neurite-based white matter alterations in MAPT mutation carriers: A multi-shell diffusion MRI study in the ALLFTD consortium.Neurobiology of aging · 2024Article
- Betz cells of the primary motor cortex.The Journal of comparative neurology · 2024Review
- 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
- Synaptic Effects of Palmitoylethanolamide in Neurodegenerative Disorders.Biomolecules · 2022Review
- A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Harnessing rAAV-retro for gene manipulations in multiple pathways that are interrupted after spinal cord injury.Experimental neurology · 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
- Differential NPY-Y1 Receptor Density in the Motor Cortex of ALS Patients and Familial Model of ALS.Brain sciences · 2021Article
- Microglia Morphological Changes in the Motor Cortex of hSOD1Brain 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
- Synaptopathy Mechanisms in ALS Caused by C9orf72 Repeat Expansion.Frontiers in cellular neuroscience · 2021Article
- Mitochondrial Fragmentation and Dysfunction in Type IIx/IIb Diaphragm Muscle Fibers in 24-Month Old Fischer 344 Rats.Frontiers in physiology · 2021Article
- Better understanding the neurobiology of primary lateral sclerosis.Amyotrophic lateral sclerosis & frontotemporal degeneration · 2020Review
- The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS.Frontiers in molecular neuroscience · 2020Article
- MCP1-CCR2 and neuroinflammation in the ALS motor cortex with TDP-43 pathology.Journal of neuroinflammation · 2019Article
- 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
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Corticospinal motor neurons (CSMN) are the cortical component of motor neuron circuitry, which controls voluntary movement and degenerates in diseases such as amyotrophic lateral sclerosis, primary lateral sclerosis and hereditary spastic paraplegia. By using dual labeling combined with molecular marker analysis, we identified AAV2-2 mediated retrograde transduction as an effective approach to selectively target CSMN without affecting other neuron populations both in wild-type and hSOD1(G93A) transgenic ALS mice. This approach reveals very precise details of cytoarchitectural defects within vulnerable neurons in vivo. We report that CSMN vulnerability is marked by selective degeneration of apical dendrites especially in layer II/III of the hSOD1(G93A) mouse motor cortex, where cortical input to CSMN function is vastly modulated. While our findings confirm the presence of astrogliosis and microglia activation, they do not lend support to their direct role for the initiation of CSMN vulnerability. This study enables development of targeted gene replacement strategies to CSMN in the cerebral cortex, and reveals CSMN cortical modulation defects as a potential cause of neuronal vulnerability in ALS.
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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.