Aims: Autophagy is an evolutionary conserved process, that is very important in neurons. Neurons are post-mitotic cells which require a strict quality control mechanism to prevent accumulation of cellular debris and ensure nutrient and energy balance. Also synapses are key elements for healthy brain functioning. The synapses of neurons are highly dynamic, especially during early period of lifetimeand. Their rate increased during embryogenesis but subsequently unnecessary synapses are eliminated through a process called pruning modulated by autophagy. Many studies have shown that autophagy is a crucial mechanism for synaptic formation, differentiation and function during neurodevelopment. In Rett Syndrome mouse models, a neurodevelopmental disease that mainly affects girls, it has been shown that pharmacologically activating autophagy, neuronal deficits and motor skills are restored. Methods: We set-up a specific protocol to enrich the synaptosomal fraction from different brain areas (cortices and hippocampi) at different developmental stages, post natal day 5 (p5) and 10 (p10). The synaptosomal fraction quality control was assessed by Western blot analysis using synapsyn 1, calnexin (endoplasmic reticulm, ER marker), TIM23 (mitochondrial marker). Results: We focused on the role of autophagy in wild-type brain development, in particular its contribution to the formation of synapses. The preliminary mass spectrometry analyses has revealed that the autophagic proteins resident in synaptosomes are differently expressed during brain devolpement. Conclusions: Our preliminary results support the hypotesis that evaluating autophagic markers involved in neuronal development, could help to identify new therapeutic targets for a variety of neurological disorders.