APOE-ε4 has been shown to be a strong genetic risk factor for amyloid pathology (e.g., β-amyloid deposition, subsequent neuroinflammation and microglia activation) in Alzheimer’s disease [23,24,25,26]; however its association with tauopathies—the typical pathological hallmark of CTE—is less clear. Here, APOE is linked to early-onset autosomal dominant Alzheimer disease.