INTRODUCTION: Parkinsons Disease (PD) is one of the most prevalent neurodegenerative disorders. α-synuclein (α-syn) aggregation in form of Lewy Bodies (LB) is present in most PD patients, thus contituting a major hallmark of this disorder. The initial Lewy pathology has already been shown to be formed in the dorsal motor nucleus of the vagus (DMV) or olfactory bulb by neuropathological studies, which makes it plausible for LBs formed in gut nerve plexuses to propagate via vagus nerve to the brain.

AIM(S): The study aims to establish the link between gut-derived α-syn aggregates and brain pathology, considering α-syn spread mechanisms, oxidative stress response and behavioral manifestations.

METHOD(S): Locomotor activity study, gene expression analysis, climbing assay, survival study, smurf assay and whole brain imaging were performed on transgenic flies expressing PD-linked α-syn[A53T] tagged with BiFC-Venus under the control of the midgut expression (mex) promoter.

RESULTS: We found no significant signal in whole brain imaging, moreover mutated flies tested negative in the Smurf assay.

CONCLUSIONS: Our results suggest that sole expression of α-syn[A53T] in the midgut does not condition its spread to the brain. Moreover, the intestinal barrier resumes intact in the experimental group.