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In mouse models of these disorders, from Alzheimer\u2019s to prion disease, modulation of the pathway\u2014including by the licensed drug, trazodone\u2014restores global protein synthesis rates with profound neuroprotective effects. However, the precise nature of the translational impairment, in particular the specific proteins affected in disease, and their response to therapeutic UPR modulation are poorly understood. We used non-canonical amino acid tagging (NCAT) to measure de novo protein synthesis in the brains of prion-diseased mice with and without trazodone treatment, in both whole hippocampus and cell-specifically.<\/jats:p>\n                  <jats:p>During disease the predominant nascent proteome changes occur in synaptic, cytoskeletal and mitochondrial proteins in both hippocampal neurons and astrocytes. Remarkably, trazodone treatment for just 2\u2005weeks largely restored the whole disease nascent proteome in the hippocampus to that of healthy, uninfected mice, predominantly with recovery of proteins involved in synaptic and mitochondrial function. In parallel, trazodone treatment restored the disease-associated decline in synapses and mitochondria and their function to wild-type levels.<\/jats:p>\n                  <jats:p>In conclusion, this study increases our understanding of how translational repression contributes to neurodegeneration through synaptic and mitochondrial toxicity via depletion of key proteins essential for their function. Further, it provides new insights into the neuroprotective mechanisms of trazodone through reversal of this toxicity, relevant for the treatment of neurodegenerative diseases via translational modulation.<\/jats:p>","DOI":"10.1093\/brain\/awad313","type":"journal-article","created":{"date-parts":[[2023,9,13]],"date-time":"2023-09-13T13:50:08Z","timestamp":1694613008000},"page":"649-664","source":"Crossref","is-referenced-by-count":29,"title":["Trazodone rescues dysregulated synaptic and mitochondrial nascent proteomes in prion neurodegeneration"],"prefix":"10.1093","volume":"147","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2028-738X","authenticated-orcid":false,"given":"Hector","family":"Albert-Gasco","sequence":"first","affiliation":[{"name":"UK Dementia Research Institute and Department of Clinical Neurosciences, University of Cambridge , Cambridge CB2 0AH , UK"},{"name":"Cambridge Institute of Science, Altos Labs , Great Abington CB21 6GP , 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Institute of Science, Altos Labs , Great Abington CB21 6GP , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Halliday","sequence":"additional","affiliation":[{"name":"Cambridge Institute of Science, Altos Labs , Great Abington CB21 6GP , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sudha","family":"Janaki-Raman","sequence":"additional","affiliation":[{"name":"Altos Labs Inc , Redwood City, CA 94065 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrian J","family":"Butcher","sequence":"additional","affiliation":[{"name":"UK Dementia Research Institute and Department of Clinical Neurosciences, University of Cambridge , Cambridge CB2 0AH , UK"},{"name":"Cambridge Institute of Science, Altos Labs , Great Abington CB21 6GP , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8504-1191","authenticated-orcid":false,"given":"Giovanna 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