Keywords: Epilepsy, Epilepsy, Temporal Lobe Epilepsy, TLE, Spectroscopy, myo-Inositol, m-Ins
Motivation: The pathophysiology of cognitive decline in TLE remains unclear, which hampers the development of new treatments.
Goal(s): To uncover new ways to anticipate and possibly prevent cognitive decline in TLE.
Approach: We used 1H-MRS to precisely track M-Ins levels in brain areas of interest, which allowed detailed insights into the relationship between brain inflammation, seizures, and thinking abilities.
Results: Patients with nonlesional TLE, whose temporal regions appear normal on MRI, show increased hippocampal myo-inositol, a marker of glial cell activation. This increase is specific to the hippocampus, not the cortex, and higher M-Ins levels correlate with poorer cognitive outcomes.
Impact: This study could significantly impact public health by revealing how brain inflammation contributes to cognitive loss in TLE. It may open doors to new treatments focused on preserving cognitive health in other epilepsy patients, potentially improving their quality of life.
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