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| http://dx.doi.org/10.4103/0974-8237.142311 | DOI Listing |
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Alterations in cardiac function correlate with a disruption in fatty acid metabolism in a mouse model of SMA.
Hum Mol Genet
January 2025
Centre for Discovery Brain Sciences, Hugh Robson Building, George Square, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom.
Spinal Muscular Atrophy is an autosomal dominant disease caused by mutations and deletions within the SMN1 gene, with predominantly childhood onset. Although primarily a motor neuron disease, defects in non-neuronal tissues are described in both patients and mouse models. Here, we have undertaken a detailed study of the heart in the Smn2B/- mouse models of SMA, and reveal a thinning of the ventriclar walls as previously described in more severe mouse models of SMA.
View Article and Find Full Text PDFMotor involvement in frontotemporal lobar degeneration with TAR DNA-binding protein of 43 kDa type C.
Neuropathology
January 2025
Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan.
The degeneration of pyramidal tracts has been reported in frontotemporal lobar degeneration with TDP-43 (TAR DNA-binding protein 43) pathology (FTLD-TDP) type C. Herein, we examined the detailed pathology of the primary motor area and pyramidal tracts in the central nervous system in four autopsy cases of FTLD-TDP type C, all of which were diagnosed by neuropathological, biochemical, and genomic analyses. Three patients showed right dominant atrophy of the frontal and temporal lobes, while the other patient showed left dominant atrophy.
View Article and Find Full Text PDFClonally expanded, targetable, natural killer-like NKG7 T cells seed the aged spinal cord to disrupt myeloid-dependent wound healing.
Neuron
January 2025
Molecular Neuroregeneration, Division of Neuroscience, Department of Brain Sciences, Imperial College London, London, UK. Electronic address:
Spinal cord injury (SCI) increasingly affects aged individuals, where functional impairment and mortality are highest. However, the aging-dependent mechanisms underpinning tissue damage remain elusive. Here, we find that natural killer-like T (NKLT) cells seed the intact aged human and murine spinal cord and multiply further after injury.
View Article and Find Full Text PDFMechanisms for dysregulation of excitatory-inhibitory balance underlying allodynia in dorsal horn neural subcircuits.
PLoS Comput Biol
January 2025
Department of Mathematics and Statistics, Middlebury College, Middlebury, Vermont, United States of America.
Chronic pain is a wide-spread condition that is debilitating and expensive to manage, costing the United States alone around $600 billion in 2010. In a common symptom of chronic pain called allodynia, non-painful stimuli produce painful responses with highly variable presentations across individuals. While the specific mechanisms remain unclear, allodynia is hypothesized to be caused by the dysregulation of excitatory-inhibitory (E-I) balance in pain-processing neural circuitry in the dorsal horn of the spinal cord.
View Article and Find Full Text PDFAmantadine modulates novel macrophage phenotypes to enhance neural repair following spinal cord injury.
J Transl Med
January 2025
Department of Neurosurgery, The Second Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, China.
Background: Spinal cord injury (SCI) triggers a complex inflammatory response that impedes neural repair and functional recovery. The modulation of macrophage phenotypes is thus considered a promising therapeutic strategy to mitigate inflammation and promote regeneration.
Methods: We employed microarray and single-cell RNA sequencing (scRNA-seq) to investigate gene expression changes and immune cell dynamics in mice following crush injury at 3 and 7 days post-injury (dpi).
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