This observational neuroimaging study from University of Turku (n=14 long COVID patients, 11 controls, 13 MS comparators; total sample 38) used TSPO-PET to rule out widespread glial activation as the driver of persistent symptoms, contrasting with earlier neuropathological reports from acute severe COVID cases. Unlike randomized trials, this cross-sectional design cannot establish causality or track longitudinal change, and no conflicts of interest were disclosed. The key positive signal—elevated hippocampal/amygdala activity correlating with anxiety, depression, and reduced quality of life—aligns with patterns seen in a 2022 Lancet Psychiatry cohort study (n=384) linking post-COVID mood dysregulation to limbic hypermetabolism rather than diffuse neuroinflammation. A 2023 JAMA Neurology meta-analysis of 1,200 long COVID cases similarly found inflammatory markers normalize after 12 months while psychiatric symptoms persist, suggesting the Turku findings may generalize. Original coverage underplayed the 16-month subgroup effect and failed to note that small-sample PET studies risk type II error when claiming absence of inflammation. Collectively these data redirect research from anti-inflammatory agents toward CBT or neuromodulation trials targeting emotional circuits.