[SCAN] Drosophila models to investigate the neurobiology of innate behaviours and neuropathologies

Title: Drosophila models to investigate the neurobiology of innate behaviours and neuropathologies

Speaker: Gonçalo Poças

Abstract: I will present two independent studies using in vivo models of Drosophila melanogaster (commonly known as fruit flies):

a) The neuronal control of energetic and macronutrient homeostasis

The search for food and its consumption is of primordial importance for animals’ survival and fitness. We are investigating the neuronal basis of the innate behaviours associated to foraging and nutritional decisions. Despite the nervous system of fruit flies being considerably simpler than that of mammals, it encodes a complex repertoire of behaviours. We have been performing suppression and activation screens that are enabling us to identify the neuronal populations associated with specific phenotypic classes associated with the regulation of food intake. By contributing to understanding how flies make nutritional decisions at the neural level, our study aims to provide general insights into how food intake is regulated in other animals and, ultimately, to contribute to uncovering the neuronal basis of human eating disorders.

b) Genipin protects against ɑ-synuclein toxicity, in the context of Parkinson’s disease

Parkinson’s Disease (PD) is a common neurodegenerative disorder in which one of the hallmarks is the aggregation and toxicity of α-Synuclein (α-Syn), a neuronal protein highly enriched in the pre-synaptic nerve terminals. Unfortunately, and despite affecting millions of people worldwide, only symptomatic therapies are currently available for PD. Small molecules able to target key pathological processes have emerged as interesting options for modifying disease progression. We identified genipin, an iridoid, which prevents several hallmarks of PD, including α-Syn aggregation, motor deficits and decreased longevity. As we still lack disease-modifying therapies for PD, and while clinical trials keep failing, we hope our study positively contributes to the urgent discovery of new sources of small molecules capable of modulating PD etiology.