Joel E. Kleinman

Apr 30, 2024 | nature.com | Leonardo Sportelli |Daniel Eisenberg |Enrico D’Ambrosio |Michael Gregory |Thomas Hyde |Joel E. Kleinman | +6 more

AbstractThe polygenic architecture of schizophrenia implicates several molecular pathways involved in synaptic function. However, it is unclear how polygenic risk funnels through these pathways to translate into syndromic illness. Using tensor decomposition, we analyze gene co-expression in the caudate nucleus, hippocampus, and dorsolateral prefrontal cortex of post-mortem brain samples from 358 individuals.