I believe the current thinking on Alzheimers and PD is that they both are considered a form of prion disease in that plaques are observed in the brain. In the article below, a case is made that anti-rejection drugs like FK506 and cyclosporine have a noticeable effect on A-synulclein and could be very useful in treating PD. See Fig. 3 bar graph. These drugs have been used for years in people with organ transplants to prevent rejection. In this article it is suggested that there is an optimal dose of FK506 to suppress A-synulein (not too little not too much) and that the drug could be taken intermittently.
It's too bad that these FDA approved drugs are not fast tracked into some sort of trial to see how effective they could be in PD and AD. Many are years into these diseases and time is running out.

Calcineurin determines toxic versus beneficial responses to α-synuclein
Because inhibition of calcineurin activity is routinely exploited clinically through the use of FK506 (tacrolimus) as an immunosuppressant, we now suggest that the repurposing of FK506, a compound that readily traverses the blood brain barrier merits investigation in the management of PD. Because it persists in the central nervous system long after systemic effects have resolved (49), intermittent dosing with this already FDA-approved drug could avoid systemic immunosuppression, while still providing a readily implemented, disease-modifying treatment strategy that targets a fundamental mechanism in the pathogenesis of α-synucleinopathies.