α-synuclein is a recently discovered protein that was first identified as the major non amyloid component of senile plaques, the cerebral lesion likely responsible for Alzheimers disease. The role of α-synuclein in another brain disease namely Parkinsons disease, has been more deeply documented. It appears that α-synuclein fills up the intracytoplasmic inclusions called Lewy bodies that likely contribute to the etiology of Parkinsons disease. Furthermore, rare familial forms of Parkinsons disease have been shown to be linked to autosomal dominant mutations of α-synucleins. Is α-synuclein a bridge between Alzheimers and Parkinsons diseases? Could it be seen as a common denominator for these two neurodegenerative diseases? These issues could be better addressed by further delineating the physiological function of α-synuclein and, as a corollary, the dysfunction taking place along with the diseases. Here, I will review the recent advances concerning the physiology of α-synuclein and will particularly focus on the post-traductional events leading to drastic biophysical transformations. I will describe recent works suggesting that these modifications directly modulate the normal function of α-synuclein, likely accounting for the dysfunction associated with Parkinsons disease and perhaps contributing to Alzheimers pathology.
Keywords: synuclein cell biology, synuclein, parkinson disease, lewy bodies
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