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10.1016/j.pneurobio.2025.102809 http://scihub22266oqcxt.onion/10.1016/j.pneurobio.2025.102809 40784541!ä!40784541 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=40784541&cmd=llinks): Failed to open stream: HTTP request failed! 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Cortical hyperexcitability drives dying forward amyotrophic lateral sclerosis symptoms and pathology in mice |pdf=|usr=}}{{40784541}} gab.com Text Cortical hyperexcitability drives dying forward amyotrophic lateral sclerosis symptoms and pathology in mice JO: Prog Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=40784541 #FOAvip Degeneration of both upper motor neurons in the brain and lower motor neurons in the spinal cord defines amyotrophic lateral sclerosis (ALS), but how they are linked in ALS pathophysiology is unclear. Here, we uncover a cortical origin of neurodegeneration in ALS mediated by upper motor neuron hyperexcitability. Chronic hyperexcitability of upper motor neurons induced by excitatory chemogenetics in healthy adult mice induced progressive motor deficits, weakness and core pathological hallmarks of ALS, including upper motor neurons loss, synaptic pathology, corticospinal tract degeneration and reactive gliosis. Importantly, upper motor neuron hyperexcitability and loss were sufficient to drive degeneration of lower motor neurons and their distal axons and neuromuscular junctions, associated with astrocyte and microglial activation in spinal cord. Cortical hyperexcitability also triggered cytoplasmic TAR DNA binding protein 43 (TDP-43) aggregation in upper motor neurons and lower motor neurons, placing hyperexcitability upstream of TDP-43 proteinopathy in ALS. These findings establish a cortical origin of ALS mediated by upper motor neurons, consistent with an anterograde mechanism of neurodegeneration throughout the central and peripheral nervous systems. Twit Text FOAVip Cortical hyperexcitability drives dying forward amyotrophic lateral sclerosis symptoms and pathology in mice ????Prog Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=40784541 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=40784541 #FOAvip English Wikipedia <ref>{{Cite pmid|40784541}}</ref> Cortical hyperexcitability drives dying forward amyotrophic lateral sclerosis symptoms and pathology in mice #MMPMID40784541 Haidar M; Viden A; Daniel C; Cuic B; Wang T; Rosier M; Tomas D; Mills SA; Govier-Cole A; Djouma E; Perera ND; Luikinga S; Rytova V; Barton SK; Gonsalvez DG; Palmer LM; McLean C; Kiernan MC; Vucic S; Turner BJ Prog Neurobiol 2025[Aug]; 252 (ä): 102809 PMID40784541show ga Degeneration of both upper motor neurons in the brain and lower motor neurons in the spinal cord defines amyotrophic lateral sclerosis (ALS), but how they are linked in ALS pathophysiology is unclear. Here, we uncover a cortical origin of neurodegeneration in ALS mediated by upper motor neuron hyperexcitability. Chronic hyperexcitability of upper motor neurons induced by excitatory chemogenetics in healthy adult mice induced progressive motor deficits, weakness and core pathological hallmarks of ALS, including upper motor neurons loss, synaptic pathology, corticospinal tract degeneration and reactive gliosis. Importantly, upper motor neuron hyperexcitability and loss were sufficient to drive degeneration of lower motor neurons and their distal axons and neuromuscular junctions, associated with astrocyte and microglial activation in spinal cord. Cortical hyperexcitability also triggered cytoplasmic TAR DNA binding protein 43 (TDP-43) aggregation in upper motor neurons and lower motor neurons, placing hyperexcitability upstream of TDP-43 proteinopathy in ALS. These findings establish a cortical origin of ALS mediated by upper motor neurons, consistent with an anterograde mechanism of neurodegeneration throughout the central and peripheral nervous systems. äCortical hyperexcitability drives dying forward amyotrophic lateral sc(epmc).pdf DeepDyve Pubget Overpricing