These were reported to either (1) inhibit the formation of oxidative species from microglia, which results in svPPA (NCT05184569); (2) modulate synaptic activity to mitigate the release of proinflammatory mediators (NCT04489017, NCT04220021) targeting bvFTD and ALS or any disease subtype on the FTD spectrum, respectively; (3) inhibit enzymes that activate transposable elements resulting in bvPPA (NCT04993755); or (4) alter post-translational modification of tau resulting in bvFTD or nfvPPA (ACTRN = 12620000236998). This evidence concerns the gene MAPT and amyotrophic lateral sclerosis.