The ATX(N) framework expands upon the traditional AT(N) biomarker model by incorporating additional biomarkers (X) that capture non-amyloid, non-tau pathologies, such as TDP-43, α-synuclein, neuroinflammation, and vascular injury, thereby better reflecting the biological heterogeneity of Alzheimer’s disease [62]. This evidence concerns the gene SNCA and Alzheimer disease.