Cognitive Reserve Delays Symptom Onset in Dominantly Inherited Alzheimer Disease

Alzheimer disease remains a leading cause of cognitive impairment and mortality in the aging population [1, 2]. While the biological definition of the disease has shifted toward a biomarker-based framework involving amyloid and tau pathology, the clinical expression of these changes varies significantly between individuals [3]. The cognitive reserve hypothesis suggests that factors such as educational attainment, physical activity, and social engagement may provide resilience against neurodegeneration [4, 5, 6]. While these modifiable factors are well-documented in sporadic Alzheimer disease, their impact on patients with high-penetrance genetic mutations has remained less clear [7]. A recent study examines whether this protective buffer can alter the clinical course of dominantly inherited Alzheimer disease, offering insights into how lifestyle and baseline cognition might delay symptoms even in patients with a predetermined genetic trajectory.