Simon Licht‐Mayer

The paper shows that TCA cycle dysfunction contributes to axonal energy deficiency in neuroinflammatory lesions and that restoring TCA enzymes can alleviate this deficit.

This study demonstrates that BH4 deficiency exacerbates PD-related stressors and that BH4 augmentation protects dopaminergic neurons in multiple models.

The paper assesses axonal mitochondrial content and complex IV activity in multiple experimental disease models of MS, finding that increased mitochondrial content does not always correlate with increased COX activity, and that COX activity inversely correlates with axonal injury.