From a drug-discovery perspective, the strongest near-term program is to separate direct tau-binding from systems-level proteostasis effects. Use recombinant aggregation and seeding assays first, then repeat the best conditions in human iPSC neurons expressing seeded tau to determine whether the mechanism scales from purified protein to disease-relevant biology.
Rutin's liabilities are familiar: limited oral bioavailability, uncertain CNS exposure, and promiscuous chemistry typical of polyphenols. That does not kill the program, but it shifts the emphasis toward analog design, formulation, or using rutin as a scaffold for a CNS-optimized derivative. The most decision-useful biomarkers are tau seeding assays, oligomer-selective ELISAs, phospho-tau panels, and unbiased proteostasis readouts that can discriminate between binding, oxidation control, and clearance enhancement.