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Since a complex microbiota was found to be necessary for worsening -synuclein pathology, it is likely that a combination of the increase in harmful bacteria, decrease in beneficial bacteria, and similar changes in their derived products trigger and facilitate -synuclein fibril formation, propagation, and disease pathology (Figure 2)

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Targeting NOS1 either through Hsp90 inhibitors to block its mitochondrial localization or via specific inhibitors such as N-propyl-L-arginine may offer dual benefits: mitigating therapy resistance and addressing metabolic risk factors in CRC (57, 58)

This does not influence the clinical analysis