The build-up of a protein called alpha-synuclein has been considered one of the hallmarks of Parkinson’s; evidence suggests alpha-synuclein may play a role in driving the loss of dopamine neurons (nerve cells) in Parkinson’s as this protein forms clumps that puts stress on cells and may lead to their death. Recently, however, a group of scientists have called into question the ‘bad guy’ role of alpha-synuclein.
Led by Professor Jeff Kordower, who sits on our International Linked Clinical Trials committee, the team analysed sections of brain tissue from a large cohort of people who had passed away and divided them into three groups based on their medical records: those who had been diagnosed with Parkinson’s; those who had minor motor symptoms of Parkinson’s but no diagnosis, and those with no motor issues.
The researchers found that alpha-synuclein deposits were not present in all the brains of people with minor motor symptoms of Parkinson’s and that there was no difference in clinical symptoms between those with alpha-synuclein clumping and those without. In addition, the researchers reported that neuron loss was not associated with alpha-synuclein build-up, suggesting alpha-synuclein may not be the only factor driving dopamine neuron loss.
Interestingly, when the researchers turned their attention to another protein, Tau, they found that it was present in the brains of almost all of the cases with motor symptoms, with or without a diagnosis of Parkinson’s. This observation led the researchers to speculate that perhaps the initiation of dopamine neuron loss in Parkinson’s may be independent of alpha-synuclein, and perhaps driven by Tau instead. Tau is most commonly associated with Alzheimer’s; similar to alpha-synuclein, abnormal copies of Tau accumulate and form clumps in the parts of the brain associated with memory, leading to neuron loss there.
Although this is an interesting finding, it will need to be replicated by other independent scientists before any conclusions can be drawn as the current consensus points to alpha-synuclein as a major driver or possible consequence of Parkinson’s progression.
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