{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSARM1 is a central regulator of axon degeneration. Upon injury or stress, SARM1 becomes activated and—via its intrinsic NADase activity located in its TIR domain—rapidly depletes NAD⁺, triggering an energetic catastrophe that leads to Wallerian degeneration. Structural studies have revealed that SARM1 assembles into a tightly regulated octamer, and its activation depends on the release of an autoinhibited state, a process influenced by factors such as NMN‐accumulation, protonation, and specific mutations. These mechanisms underlie its roles in diverse contexts including traumatic nerve injury, chemotherapy‐induced peripheral neuropathy, spinal cord injuries, and even neuroinflammatory processes in the enteric nervous system where axon loss can be beneficial to dampen local inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, SARM1 activity is precisely controlled through intramolecular interactions that maintain an autoinhibited conformation. Cryo–electron microscopy has demonstrated that binding of NAD⁺ to the inhibitory ARM domain prevents premature TIR-domain dimerization and catalytic activation. Moreover, regulatory inputs such as acidification and phosphorylation—mediated by kinases like JNK—can perturb these interactions, lowering the activation threshold and promoting enzymatic activity. These studies highlight the complex structural regulation that ensures SARM1 is only unleashed under conditions of bona fide cellular stress."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in axonal self‐destruction, SARM1 functions in non‐neuronal contexts as well. It serves as a negative regulator in Toll–like receptor signaling, where it downmodulates both TRIF– and MyD88–dependent pathways, thereby curbing excessive inflammatory responses. In immune cells and T lymphocytes, SARM1 has been implicated in promoting intrinsic apoptosis via mitochondrial and even nuclear mechanisms, sometimes through interactions with partners such as retinoschisin, UXT, and PINK1/TRAF6 complexes that influence mitophagy. Such multifaceted roles underscore SARM1’s importance not only in neurodegeneration but also in the broader regulation of cell death and innate immunity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, aberrant SARM1 activity is emerging as an important determinant in neurodegenerative and neuroinflammatory disorders. Rare patient‐specific gain–of–function variants confer hyperactive NADase activity and are associated with conditions such as amyotrophic lateral sclerosis and other motor neuropathies, while loss–of–function alleles appear to mitigate axonal loss. In addition, dysregulation of SARM1 has been linked to adverse responses in chemotherapy–induced neuropathy and to pathological changes in the context of spinal cord injury. SARM1 signaling is also modulated by non–coding RNAs in cancer, as demonstrated in prostate cancer models, highlighting its potential as a versatile therapeutic target across a spectrum of human diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Laura Conforti, Jonathan Gilley, Michael P Coleman "}, {"type": "b", "children": [{"type": "t", "text": "Wallerian degeneration: an emerging axon death pathway linking injury and disease."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Rev Neurosci (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/nrn3680"}], "href": "https://doi.org/10.1038/nrn3680"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24840802"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24840802"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Josiah Gerdts, Daniel W Summers, Jeffrey Milbrandt, et al. 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