Recently, the brain’s CP activation for recruitment of inflammation-resolving monocytes and T lymphocytes attenuated Alzheimer’s disease (AD) pathology or disease progression in ALS model following glatiramer acetate [40] or myelin-derived peptide [13] immunization, with concomitant Th1-cytokine IFN-γ upregulation in the periphery. The gene discussed is IFNG; the disease is early-onset autosomal dominant Alzheimer disease.