Additional support for the aetiopathogenic role of the neuroimmune–neuroinflammation axis AD comes from genetic studies: genome-wide association studies (GWASs) reveal that multiple polymorphisms associated with AD occur in genes that regulate innate immune function (e.g., CD33, CLU, CR1, TREM-2), which encode proteins that regulate complement activation and cellular phagocytic activities [9]. The gene discussed is TREM2; the disease is Alzheimer disease.