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A cell-permeant mimetic of NMN activates SARM1 to produce cyclic ADP-ribose and induce non-apoptotic cell death

The incidence is higher in men than women.[18] According to different studies, there are 100 750 cases/100,000 individuals.[7,8,20,40,62,66] According to the Glasgow coma scale [Figure 2], we can classify TBI as: mild (1315), moderate (912), or severe (38).[33,90] Mild TBI (mTBI), the most prevalent kind of TBI (representing 70% of cases), has good survival rates, but up to 5 million Americans live with persistent TBI-related disabilities, including social, motor and cognitive dysfunctions, mood disorders, sleep disturbances, and personality changes.[13,18,19,27] Severe or recurrent TBI dramatically increases the risk of neurodegeneration, dementia, stroke, and epilepsy.[105] The primary injury in TBI can lead to focal and diffuse brain damage, which often coexist in moderate-to-severe cases.[61] However, diffuse axonal injury (DAI), which accounts for around 70% of TBI cases, is the most prevalent injury pattern.[86] The damage alters the axonal cytoskeleton and disrupts axonal transport.[76] The secondary damage is frequently delayed and protracted, and multiple variables, including excitotoxicity, mitochondrial dysfunction, oxidative stress, lipid peroxidation, neuroinflammation, axon degeneration, and apoptosis, play a role in it.[72] 24 h post-TBI, the BBB shows signs of malfunctioning, allowing circulating leukocytes to infiltrate the damaged brain parenchyma and release proinflammatory cytokines such as Interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNFa), and complement factors.[5,25,46] Neurological impairments, increased BBB permeability, and sustained overexpression of cytokines are all linked

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