http://www.northwestneurology.net/sc...nson-patients/


After analyzing cells and postmortem brain tissue from animals and humans, researchers noted that oxidative stress—a known culprit in neuron death—activated the protein tyrosine kinase c-Abl in the nigra-striatum area of the brain. Neurons in this part of the brain are particularly vulnerable to Parkinson disease injury.

Activation of this protein led to changes in the parkin protein, which is known to be mutated in hereditary Parkinson disease. The altered parkin lacked the capacity to break down other proteins, leading to harmful clumps of unprocessed protein in the neuron. The scientists believe this accumulation leads to progressive neuron death, resulting in Parkinson symptoms that worsen over time.

“When we blocked tyrosine kinase c-Abl activation, parkin function was preserved and neurons were spared,” Dr Imam said. “We believe these studies provide sound rationale for moving forward with a preclinical trial of tyrosine kinase c-Abl inhibitors, with the goal of developing a potent therapeutic drug for slowing the progression of Parkinson’s.”

If preclinical trials in animal models of Parkinson disease yield positive results, the next step would be clinical trials in human patients, Dr Imam said.

Tyrosine kinase c-Abl inhibitors are approved by the FDA for treating myeloid leukemia and gastrointestinal tumors. This could speed approval of the drug for Parkinson disease and its translation from bench research to clinical practice.