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Importantly, aberrant Cdk5 activation causes mitochondrial defects and motor neuron degeneration, as the genetic knockout of\n                    <jats:italic>p35<\/jats:italic>\n                    in an SMA mouse model rescues mitochondrial transport and fragmentation defects, and alleviates SMA phenotypes including motor neuron hyperexcitability, loss of excitatory synapses, neuromuscular junction denervation, and motor neuron degeneration. Inhibition of the Cdk5 signaling pathway reduces the degeneration of motor neurons derived from SMA mice and human SMA iPSCs. Altogether, our studies reveal a critical role for the aberrant activation of Cdk5 in SMA pathogenesis and suggest a potential target for therapeutic intervention.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2300308120","type":"journal-article","created":{"date-parts":[[2023,11,17]],"date-time":"2023-11-17T13:27:09Z","timestamp":1700227629000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":5,"title":["Mitigating aberrant Cdk5 activation alleviates mitochondrial defects and motor neuron disease symptoms in spinal muscular atrophy"],"prefix":"10.1073","volume":"120","author":[{"given":"Nimrod","family":"Miller","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611"},{"name":"Stanley Manne Children's Research Institute, Ann and Robert H. 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