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Comment & Response
January 2019

On Mediation Models in Clinical Neurology Studies—Reply

Author Affiliations
  • 1Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
  • 2Neuroscience Center, Samsung Medical Center, Seoul, Korea
  • 3Statistics and Data Center, Samsung Medical Center, Seoul, Korea
  • 4Department of Clinical Research Design and Evaluation, SAIHST, Sungkyunkwan University, Seoul, Korea
JAMA Neurol. 2019;76(1):117. doi:10.1001/jamaneurol.2018.3887

In Reply We appreciate the comments of Cogo-Moreira and Swardfager on our path analyses.1 We agree with their first comment that there is always a possibility that other factors that are not included in our model may link the predictor (Aβ positivity or cerebral small vessel disease [CSVD]) and the outcome (Mini-Mental State Examination [MMSE]) (see Figure 3 of our article1). Considering possible unmeasured factors, power issues, and that the mediation did not explain most of the observed total effects, it may not be appropriate to conclude the complete mediation in our pathway. However, we used the term “complete mediation” according to previous literature,2 as the direct association was no longer significant when the mediator (tau) was added to the model. Indeed, a substantial portion (45.9% and 61.4% for the top and bottom model of Figure 3, respectively) was explained by the mediator (tau), which is likely to be of clinical relevance.

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