Blocking key enzyme may halt PD symptoms and support use of Nilotinib
 

Researchers at Johns Hopkins say they have gleaned two important new clues in the fight against Parkinson's disease: that blocking an enzyme called c-Abl prevents the disease in specially bred mice, and that a chemical tag on a second protein may signal the disorder's presence and progression. Their work, described online June 27 in The Journal of Clinical Investigation, suggests both a promising target for drug research and a tool that could speed Parkinson's disease research more broadly, they say.

There were indications that c-Abl activity leads to Parkinson's disease, and our experiments show there is indeed a connection," says Ted Dawson, M.D., Ph.D., professor of neurology and director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. "There is already a Food and Drug Administration-approved c-Abl inhibiting drug in use for leukemia," he adds, "so we're interested in whether it could be used safely against Parkinson's disease or as a starting point to develop other treatments.

.....Dawson and Ko caution that the use of the anti-leukemia drug nilotinib is not yet indicated for Parkinson's disease patients and that further studies are needed before their results can be applied to clinical care.

Blocking key enzyme halts Parkinson's disease symptoms in mice

I find it very frustrating that there is an approved drug on the market, which has been shown to be effective for treating PD, yet researchers can't get funding to conduct the required clinical trials. Yes, we all are aware of the many limitations associated with the research conducted at Georgetown. But, isn't this the way research is supposed to proceed. A small, proof of concept study shows some efficacy, which leads to, controlled trials. I can't understand why it's been so difficult to get funding. But, I intend to find out.

This looks promising. There is a free-access version of the paper here; JCI -
Activation of tyrosine kinase c-Abl contributes to α-synuclein–induced neurodegeneration.

Abl is a tyrosine protein kinase. What the authors showed is that Abl-mediated phosphorylation of Tyr39 of α-synuclein led to neurodegeneration in a mouse model of PD, probably arising from aggregation of α-synuclein. They also found elevated levels of phosphorylated α-synuclein at Tyr39 in post-mortem examination of people with PD, compared to age-matched controls.

Inhibition of a protein tyrosine kinase activity in Plasmodium falciparum by chloroqu
 

I think above study about effects of "Nilotinib" for PD, could confirm the effects of anti-malaria drug (chloroquine) in PD. Or both could confirm together . but the key is that "chloroquine" is more cheaper drug.

This study shows that chloroquine is acting as an Tyrosine kinase inhibitor in malaria diseas:
Inhibition of a protein tyrosine kinase activity in Plasmodium falciparum by chloroquine.
Inhibition of a protein tyrosine kinase activity in Plasmodium falciparum by chloroquine. - PubMed - NCBI

In other hand , researches shows that antimalarial drug "chloroquine" has good effects on PD.
Anti-Malaria Drugs May Hold Promise as Parkinson’s Treatments
- Jul 23 2015
Anti-Malaria Drugs May Hold Promise as Parkinson’s Treatments - Parkinson's Disease Foundation (PDF)

Best Wishes

All the soldiers who went to Viet Nam took a weekly dose of 500 mg of chloroquine phosphate for malaria prophylaxis. This would have been for at least a year.

It would be nice to see if quinine, artemisinin, or a host of Amazon rain forest
herbs that affect malaria would act the same way as chloroquine in PD.