These findings are consistent with the hypothesis that dysregulated expression of constitutively expressed AMPs like hBD-1 [32], specific inducible hBDs, including hBD-2 and-3, and perhaps other AMPs such as LL-37 [33], all potential modulators of inflammation, may occur in the traumatized brain and in brain tissue exhibiting chronic inflammation-associated neurodegeneration, as is observed in AD. This evidence concerns the gene ADSL and Alzheimer disease.