In particular, targeting pathways that are known to be dysregulated in AD—such as TGF-β signalling, Toll-like receptor signalling, or more broadly excessive microglial and astrocyte activation and gliosis—but that are currently not being explored in favour of Amyloid-targeting therapies may prove a more fruitful approach to therapeutics given the difficulties in finding effective Amyloid-targeting therapies. Here, TGFB1 is linked to Alzheimer disease.