Genetic risk for Alzheimer disease affects the brain throughout the lifespan

Neuronal cell death and loss of synapses are hallmarks of the pathology of Alzheimer disease (AD). The incidence of AD increases with age, and both regional and global brain atrophies have been identified as pathological correlates. Thus, AD can, in many respects, be regarded as a paradigmatic neurodegenerative disorder. However, disrupted function of the presenilin genes, the most common cause of early-onset familial AD (FAD), can also affect brain development, including early processes of neuronal migration and morphogenesis.(1)