{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gilley J"],"funding":["Medical Research Council","Motor Neurone Disease Association","Biotechnology and Biological Sciences Research Council"],"pagination":["10-16"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5640801"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["Studies with the Wld<sup>S</sup> mutant mouse have shown that axon and synapse pathology in several models of neurodegenerative diseases are mechanistically related to injury-induced axon degeneration (Wallerian degeneration). Crucially, an absence of SARM1 delays Wallerian degeneration as robustly as Wld<sup>S</sup>, but their relative capacities to confer long-term protection against related, non-injury axonopathy and/or synaptopathy have not been directly compared. While Sarm1 deletion or Wld<sup>S</sup> can rescue perinatal lethality and widespread Wallerian-like axonopathy in young NMNAT2-deficient mice, we report that an absence of SARM1 enables these mice to survive into old age with no overt phenotype, whereas those rescued by Wld<sup>S</sup> invariantly develop a progressive neuro"],"journal":["Cell reports"],"pubmed_title":["Sarm1 Deletion, but Not Wld<sup>S</sup>, Confers Lifelong Rescue in a Mouse Model of Severe Axonopathy."],"pmcid":["PMC5640801"],"funding_grant_id":["RIBCHESTER/APR15/838-791","BBS/E/B/000C0433","MR/M024075/1","MR/N004582/1","G1000702"],"pubmed_authors":["Ribchester RR","Coleman MP","Gilley J"],"additional_accession":[]},"is_claimable":false,"name":"Sarm1 Deletion, but Not Wld<sup>S</sup>, Confers Lifelong Rescue in a Mouse Model of Severe Axonopathy.","description":"Studies with the Wld<sup>S</sup> mutant mouse have shown that axon and synapse pathology in several models of neurodegenerative diseases are mechanistically related to injury-induced axon degeneration (Wallerian degeneration). Crucially, an absence of SARM1 delays Wallerian degeneration as robustly as Wld<sup>S</sup>, but their relative capacities to confer long-term protection against related, non-injury axonopathy and/or synaptopathy have not been directly compared. While Sarm1 deletion or Wld<sup>S</sup> can rescue perinatal lethality and widespread Wallerian-like axonopathy in young NMNAT2-deficient mice, we report that an absence of SARM1 enables these mice to survive into old age with no overt phenotype, whereas those rescued by Wld<sup>S</sup> invariantly develop a progressive neuro","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2025-04-22T21:15:59.961Z","creation":"2019-03-27T02:58:58Z"},"accession":"S-EPMC5640801","cross_references":{"pubmed":["28978465"],"doi":["10.1016/j.celrep.2017.09.027"]}}