Hi Iain

Just to chime in if you don’t mind!

Would the intercept be a column of 1s?
However, this analysis won’t tell us whether the relationship is specific to the patients, right?




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On Saturday, May 25, 2019, 10:33 pm, Anderson M. Winkler <[log in to unmask]> wrote:

Hi Iain,

You can do the TBSS analysis in which you investigate the association between RT and AD, while having the groups (patients and controls) as nuisance. The model would be:

EV1: RT
EV2: groups (coded as +1/-1)
EV3: intercept.

All the best,

Anderson


On Wed, 22 May 2019 at 07:02, Iain Croall <[log in to unmask]> wrote:
Hello experts,

I've got some DTI data that I've done a TBSS experiment with, comparing a patient population against matched controls. This shows some widespread significant differences in axial diffusivity. There's also cognitive data for all subjects, from which I know the patients are impaired in a reaction time task compared to the controls.

I'd like to correlate the TBSS with the reaction time task. My question at the heart of this would be to ask if the physiological difference between groups (the TBSS AD change) is a driver of the cognitive difference between the groups (the cog. functioning reaction time difference). I'm conscious that simply including the reaction time values in a correlation with TBSS data will undoubtedly produce many significant results simply by virtue of this being linked to WM tract health in any situation. i.e. there will be normal "control" correlations there, and I want to separate that out to see if the damage has led to the loss of reaction time.

A) One idea would be to restrict a TBSS correlation analysis between the AD maps and cog. scores to just the patients, and then try and match up significant locations with where I know AD has changed. But I feel this still doesn't address the issue of how much those relationships were there "anyway".

B) Is there some kind of GLM model mixture that would more efficiently answer the question?

Thanks in advance for any help,
Iain

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