New research carried out by scientists at the University of Alabama could mean that we’re one step closer to developing a treatment to slow down the progression of Parkinson’s disease. During their study, the researchers discovered that a mutant gene interacts with the alpha synuclein in neurons to cause the typical pathologies seen in the disease. These findings give rise to hope that new mechanisms and targets for neuroprotection can be found, particularly as they’ve identified that specific drugs currently under development may have the ability to block this process.
One of the main findings to come out of the study was the part played by a mutant LRRK2 kinase enzyme in causing alpha synuclein protein inclusions to form within the neurons. The research also indicated that two LRRK2 kinase inhibitor drugs, which are currently under development, are able to prevent the formation of these inclusions.
From their findings, the team concluded that understanding more about this interaction may lead to the discovery of new mechanisms and targets for neuroprotection, particularly as their results have demonstrated that the inclusion formation can be blocked. Therefore, it’s highly likely that these new drugs will be able to slow down the progression of the pathology associated with Parkinson’s, and therefore slow down the progression of the disease itself.
While the new drugs need to be tested in other preclinical models of Parkinson’s disease, the data does give hope that they will prove to be an effective therapy for the disease. The researchers believe that the LRRK2 kinase inhibitors have the ability to slow down the spread of pathological alpha-synuclein, not only in patients with this particular mutation, but in all people diagnosed with Parkinson’s. However, further studies will need to be undertaken to validate both the efficacy and safety of the drugs before human clinical trials are carried out.
While alpha-synuclein is associated with Parkinson’s, it’s also seen in the development of dementia with Lewy bodies, Alzheimer’s and other forms of neurodegenerative disorders.
The research was published in a recent edition of the online Journal of Neuroscience.