To break down toxic proteins more quickly, immune cells in the brain can join together to form networks when needed. However, in certain mutations that can cause Parkinson's disease, this cooperation is impaired.
Levodopa, or L-dopa, is considered the most effective treatment for Parkinson's disease today. After a few years of treatment, however, almost all patients develop a debilitating side-effect called L-dopa induced dyskinesia, or LID, which causes involuntary movements in the limbs, face, and torso. Deep brain stimulation can alleviate LID, but the procedure is highly invasive and not all patients are eligible.
Researchers have shown that two lab-developed and nasally-delivered peptides helped slow the spread of alpha-synuclein in mice. 'If these results can be replicated in patients, it would be a remarkable advance in the treatment of devastating neurological disorders,' says the lead author.
Participants in the SURE-PD3 clinical trial showed that elevating the natural antioxidant urate through inosine treatment over two years produced no significant difference in the rate of Parkinson's disease progression.
The neurotransmitter dopamine influences the activity of a wide variety of brain areas. A deficiency of this substance can have drastic consequences: The death of dopamine-producing nerve cells in the substantia nigra - a particularly sensitive part of the brain - is what causes the core symptoms of Parkinson's disease. An international team has now investigated the role played by the transcription factor BCL11A in mice and human cells. If this important factor is missing, the neurons are even more sensitive and more likely to die. The researchers suspect that BCL11A plays a protective role for neurons.