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In the context of AD, where neuroinflammation and neurotoxicity are prominent pathological hallmarks, the modus operandi of NLY01 offers a potential therapeutic avenue to mitigate analogous pathological mechanisms inherent to this neurodegenerative condition

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According to survey data from the United States, as many as 40% of survivors with severe TBI will experience long-term disability, preventing and disrupting individual development [4]

Gene expression studies reveal modulation of 408 neuronal genes, including dramatic increases in OPRM1 (opioid receptor, up 1,294%), KCND1 (up 845%), and SLC8A2 (up 737%)

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