Measures of cognitive function in childhood and early adulthood predict later risk ( 4, 19). Studies have shown that Alzheimer’s polygenic risk score also predicts correlates of Alzheimer’s disease risk, including memory decline ( 15) and structural perturbations in the hippocampus ( 2, 16– 18), in adults without dementia. Neuropathological features can appear decades before disease onset. The sum of the alleles associated with a certain trait for a given p value threshold, weighted by their effect sizes estimated from GWAS, is called polygenic risk score.Įvidence of a slowly evolving course in Alzheimer’s disease arises from various sources. Even though these variants have a low impact on Alzheimer’s disease risk individually, the additive effect of several loci may have significant predictive utility ( 14). Studies of specific genetic risk factors have identified the apolipoprotein E (APOE) ε4 allele ( 7) and multiple other risk factors of smaller effect size detected in genome-wide association studies (GWAS) ( 8– 13). Heritability in Alzheimer’s disease has been estimated to be in the range of 48%–79% ( 5, 6). The present study evaluated early-life signs of developmental risk for Alzheimer’s disease by examining associations among genetic risk, cognition, and brain structure in children and adolescents. In fact, evidence suggests that this process begins in early life ( 4), much like other chronic disorders of adults, including obesity and cardiovascular disease. No effective treatments exist, perhaps because Alzheimer’s disease is diagnosed relatively late in a slowly evolving disease process ( 2, 3). Alzheimer’s disease is a late-life neurodegenerative disorder affecting 1 in 9 Americans over age 65 ( 1).

Atlas recall beta win 7