Assessing potential correlation between T2 relaxation and diffusion of lactate in the mouse brain

Purpose While diffusion and T-2 relaxation are intertwined, little or no correlation exists between diffusion and T-2 relaxation of intracellular metabolites in the rodent brain, as measured by diffusion-weighted MRS at different TEs. However, situation might be different for lactate, since it is present in both extracellular and intracellular spaces, which exhibit different diffusion properties and may also exhibit different T-2. Such a TE dependence would be crucial to account for when interpreting or modeling lactate diffusion. Here we propose to take advantage of a new diffusion sequence, where J-modulation of lactate is canceled even at long TE, thus retaining excellent signal, to assess potential T-2 dependence on diffusion of lactate in the mouse brain. Methods Using a frequency-selective diffusion-weighted spin-echo sequence that removes J-modulation at 1.3 ppm, thus preserving lactate signal even at long TE, we investigate the effect of TE between 50.9 and 110.9 ms (while keeping diffusion time constant) on apparent diffusivity and kurtosis in the mouse brain. Results Regardless of the metabolites, no difference appears for the diffusion-weighted signal attenuation with increasing TE. For lactate, apparent diffusivity and kurtosis remain unchanged as TE increases. Conclusion No significant TE dependence of diffusivity and kurtosis is measured for lactate in the 50-110 ms TE range, confirming that potential T-2 effects can be ignored when interpreting or modeling lactate diffusion.

Automated summary

Diffusion and T-2 relaxation in the rodent brain show little or no correlation for intracellular metabolites, except for lactate which exhibits different diffusion properties. A new diffusion sequence is used to investigate the potential T-2 dependence on lactate diffusion in the mouse brain, and it is found that there is no significant TE dependence of diffusivity and kurtosis for lactate.