These findings support a model of early reactive gliosis in pediatric FRDA, indexed by elevated mI and occurring without statistically significant neuronal loss, (acknowledging that significant reductions in tNAA may require larger samples to resolve), and extend prior cerebellar-focused work to the primary motor cortex. While GSH and GABA + did not differ between groups, the observed mI elevations highlight myo-inositol as a practical in vivo biomarker of astrocytic activation and a candidate marker for disease progression in FRDA. Longitudinal studies are needed to confirm its sensitivity to clinical trajectory and therapeutic response.
Tuesday, March 10, 2026
Myo-inositol elevation as an in vivo marker of reactive gliosis in pediatric Friedreich Ataxia: evidence from HERMES-edited MR spectroscopy
William Gaetz, Muhammad G. Saleh, Charlotte Birnbaum, Luke Bloy, Timothy P.L. Roberts, David R. Lynch, Myo-inositol elevation as an in vivo marker of reactive gliosis in pediatric Friedreich Ataxia: evidence from HERMES-edited MR spectroscopy, NeuroImage: Clinical, 2026, 103983, ISSN 2213-1582, doi:10.1016/j.nicl.2026.103983.
