Parkinson’s Disease Stopped in Animal Model: Molecular ‘Tweezers’ Break Up Toxic Aggregations of Proteins
Millions of people suffer from Parkinson’s disease, a disorder of the nervous system that affects movement and worsens over time. As the world’s population ages, it’s estimated that the number of people with the disease will rise sharply. Yet despite several effective therapies that treat Parkinson’s symptoms, nothing slows its progression.
While it’s not known what exactly causes the disease, evidence points to one particular culprit: a protein called α-synuclein. The protein, which has been found to be common to all patients with Parkinson’s, is thought to be a pathway to the disease when it binds together in “clumps,” or aggregates, and becomes toxic, killing the brain’s neurons.
Now, scientists at UCLA have found a way to prevent these clumps from forming, prevent their toxicity and even break up existing aggregates.
There are currently more than 30 diseases with no cure that are caused by protein aggregation and the resulting toxicity to the brain or other organs, including Parkinson’s, Alzheimer’s and Type 2 diabetes. It is therefore critical, Bronstein said, to find a way to stop this aggregation process. Over the last two decades, researchers and pharmaceutical companies have attempted to develop drugs that would prevent abnormal protein aggregation, but so far, they have had little or no success.