Alpha-synuclein is a neuronal protein that is implicated in several neurodegenerative diseases, including Parkinson’s disease (PD), which is the most prevalent one after Alzheimer’s disease. The societal burden of the neurodegenerative diseases is significant, and is projected to increase substantially with the aging of the population worldwide. Because neurodegenerative diseases are incurable, and are often diagnosed when damage to the brain is already extensive, it is important to understand what promotes their initiation, with the aim of preventing them. Recent thinking suggests that an initiating factor for many of these diseases is the derailment of the communication points between the cells that make up the brain. To realize how this occurs, we need a deep understanding of the normal (physiological) manner in which the cells in the brain communicate. Perplexingly, we know very little about the physiological function of alpha-synuclein, mostly because previous attempts to uncover its function have yielded contradictory results. Here we suggest that alpha-synuclein exhibits different properties under different conditions. Taking this idea into account, we propose to reexamine its function. An interesting tool in our arsenal is our discovery of functional differences between alpha-synuclein in humans and in mice. Using molecular techniques, we will examine which parts of alpha-synuclein impart on it “mouse” rather than “human” properties, and in this way will be able to dissect its functions. This new information may contribute towards the development of means to avert the breakdown in communications which eventually may lead to neurodegeneration.
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- United States-Israel Binational Science Foundation (BSF)