2018), this supports our premise that AD does not have a causal influence on MD. Second, the AD genetic instrument showed different associations between the traits tested: significant causal effect with respect to AC scales, while no effect on MD. Third, the genetic-correlation results indicated that AD is informative of the pleiotropy (mediated or horizontal) with ACQ and MD. Therefore, although the AD GWAS has a smaller sample size than the other GWAS used in the present analysis, it is informative of AD polygenic architecture as indicated by quantifiable and statistically significant SNP-based heritability and genetic correlation results. In particular, MD showed a much stronger genetic correlation with AD than that observed with AC scales. However, we note that larger AD and MD datasets will be required to confirm the current findings using genetic instruments based on genetic variants that reached the more conservative genome-wide significance threshold.
