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After mechanical damage to the brain (secondary injury), the release of excitatory amino acids such as glutamate causes excessive stimulation of the N-methyl-D-aspartate (NMDA) receptor

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NAD+ PRECURSORS (NMN, NR, NA) Both approaches enhance NAD+-dependent metabolism but through distinct mechanisms: NAD+ precursors (NMN, NR): Provide substrate for NAD+ synthesis, increasing NAD+ production 5-Amino-1MQ: Inhibits NAD+ depletion by suppressing NNMT, preserving existing NAD+ These approaches are mechanistically complementary

Tetramerization forces the N-terminal threading arms from the arm-exchanged dimer to cover the heme active site for the other pair of dimers and suggests that catalase fits the more general pattern of domain swapping with the arm-exchange being a later, tetramer-dependent elaboration