Alpha-Synuclein Pathology in Parkinson’s Disease


Alpha-synuclein (α-synuclein) is one of the three members of the synuclein family, small proteins that are present in human brains and whose normal function there is not yet completely known or understood…  What  is known is that accumulations of α-synuclein accumulate in the neurons of Parkinsonian brains over the course of the disease.. The pathological mechanism behind exactly how α-synuclein  forms the aggregates found in Lewy bodies (named for the German neurologist, Friedrich Lewy,  who first described them) has not been understood.  Animal models of this disease have not been found or as yet developed to help researchers study this disease.

But now a group of researchers from the German Center for Neurodegenerative Diseases in Bonn, Germany under the direction of Professor Donato DiMonte have developed an experimental model in rats that may help to explain how α-synuclein, or abnormal forms of α-synuclein, spread throughout the brain, and lead to finding ways to slow or even stop its progression and the progression of Parkinson’s disease.

In human pathology it has been noted that α-synuclein production usually starts in the lower regions of the brain, in the medulla oblongata,  and with the progression of the disease moves to higher regions where it accumulates gradually.  It appears to follow a typical pattern which was thought to pass through a pathway of interconnected neurons, but until now, there was no way to visualize this process.

Dr. DiMonte thinks that since there is good reason to believe that Parkinson’s actually starts in the medulla oblongata and because it is a very difficult region to reach surgically, this rat model would help solve some of the issues.

Dr. DiMonte’s group developed a viral particle carrying a human DNA form of α-synuclein and injected it into the vagus nerve in the rats’ neck.  The genetic code for the human α-synuclein passed into the rats’ neurological system and into the medulla oblongata where it began producing high quantities of human α-synuclein.  After two months, they found the α-synuclein that originated in the medulla oblongata migrated to other higher areas of the rats’ brains. Over more time, the concentrations of α-synuclein actually increased, mimicking the pathology seen in Parkison’s.  They were able to map the specific nerve tracts and note the morphological changes in the nerve projections that absorbed the human α-synuclein.

This is an exciting first study that will lead to better understanding of the progression of not only Parkinson’s disease, but other diseases such as Alzheimers that have an accumulation of α-synuclein.  Future studies could lead to therapeutic treatments that target either the production of α-synuclein or its accumulation and transmission to regions in the brain.


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