Parkinson’s disease (PD) is characterized by degeneration and loss of neurons, particularly those crucial for coordination of movements. Studies have shown that by the time the symptoms appear, people with Parkinson’s have lost 60% to 80% of their dopamine producing cells. According to the Michael J. Fox Foundation, the degeneration and loss of neurons is the pathological hallmark of Parkinson’s.
Alpha synuclein is an abundant protein in the brain especially in the presynaptic terminal of neurons. It plays a role in maintaining vesicles for the neurotransmitters in the nerve endings. There has been significant research in the areas of preventing excess alpha synuclein formation or clumping and disruption of the already existing clumps.
According to NIH Genetics Home Reference, there are genes known to predispose for Parkinson’s: Approximately 15% of people with Parkinson’s disease have a family history of this disorder. Familial cases of Parkinson’s disease can be caused by mutations in the LRRK2, PARK2, PARK7, DJ-1, PINK1, SNCA, or TMEM230 gene, or by alterations in genes that have not been identified. Mutations in some of these genes may also play a role in cases that appear to be sporadic (not inherited) alterations in certain genes, including GBA (associated with Gaucher disease, see relationship between Gaucher disease and Parkinson’s disease) and UCHL1, which do not cause Parkinson’s disease but appear to modify the risk of developing the condition in some families. Variations in other genes that have not been identified probably also contribute to Parkinson’s disease risk.
Mannitol, a common low calorie sweetener, determined by the FDA to be generally recognized as safe (GRAS) food additive – see link to FDA site and link to EFSA site – has shown that it can prevent alpha synuclein clumping in pre-clinical studies conducted by Professor Daniel Segal and Professor Ehud Gazit at Tel Aviv University in Israel, in collaboration with Professor Eliezer Masliah at University of California, San Diego.
Their publication, showed that in the test tube Mannitol was effective in preventing formation of alpha-synuclein aggregates, which are known to cause Parkinson. Furthermore, they used transgenic fruit-flies, which were genetically engineered to have alpha-synuclein aggregates in their brain, and fed them with Mannitol starting at early stages of their life cycle and throughout adulthood. This resulted in markedly less aggregates of alpha-synuclein in the brains of the flies, compared with flies that did not receive Mannitol, and was accompanied by significant amelioration of their motor deficits.
Considering together, these results suggest that Mannitol may have a preventive effect on Parkinson’s.
The researchers also examined the effect of Mannitol in Parkinson’s mice model. Note, Mannitol was administered to the mice when they already began to develop alpha-synuclein aggregates, and not before. Therefore, the mice experiments were not designed specifically to test Parkinson’s prevention.