Back

An APOE*4-Informed Genomic Atlas of the X Chromosome in Alzheimer's Disease

Cook, N.; Zeng, Y.; Yang, C.; Jiang, Z.; Wang, T.-C.; Le Guen, Y.; Cody, K.; Johnson, M.; Zhang, R.; Merritt, V. C.; Hauger, R. L.; The VA Million Veteran Program, ; FinnGen, ; Koran, M. E.; Mormino, E. C.; Gordon, B.; DeCasien, A.; Andrews, S. J.; Dumitrescu, L.; Archer, D. B.; Hohman, T. J.; Pottier, C.; Cruchaga, C.; Sherva, R.; Logue, M.; Napolioni, V.; Greicius, M. D.; Belloy, M. E.

2026-05-06 neurology
10.64898/2026.05.05.26352461 medRxiv
Show abstract

The genetic contributions of the X chromosome to Alzheimers disease (AD) remain poorly understood yet are expected to importantly shape sex differences in AD. We therefore performed large-scale X-chromosome-wide association studies (N=1,240,451), evaluating differential risk due to sex, APOE*4, and escape from X-chromosome inactivation, finding most X-linked loci appear relevant to female-biased AD etiology. In evaluating genetic pleiotropy with hormonal, lipid, and brain imaging traits, we discovered X-linked AD loci converged on white matter traits, particularly in the anterior corona radiata and splenium of the corpus callosum. Through brain-centric functional genomics analyses, we then nominated candidate causal genes, including 5 that appeared highly robust. Notably, we found the escape gene RBBP7 decreases AD risk in APOE*4 carriers likely through higher expression in excitatory neurons to counter tau-related neurodegeneration. Altogether, we provide an atlas of sex and APOE*4-informed candidate X-linked AD risk loci, genes, and mechanisms that will guide future studies.

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.