In Journal of personalized medicine
The wide spectrum of unique needs and strengths of Autism Spectrum Disorders (ASD) is a challenge for the worldwide healthcare system. With the plethora of information from research, a common thread is required to conceptualize an exhaustive pathogenetic paradigm. The epidemiological and clinical findings in ASD cannot be explained by the traditional linear genetic model, hence the need to move towards a more fluid conception, integrating genetics, environment, and epigenetics as a whole. The embryo-fetal period and the first two years of life (the so-called 'First 1000 Days') are the crucial time window for neurodevelopment. In particular, the interplay and the vicious loop between immune activation, gut dysbiosis, and mitochondrial impairment/oxidative stress significantly affects neurodevelopment during pregnancy and undermines the health of ASD people throughout life. Consequently, the most effective intervention in ASD is expected by primary prevention aimed at pregnancy and at early control of the main effector molecular pathways. We will reason here on a comprehensive and exhaustive pathogenetic paradigm in ASD, viewed not just as a theoretical issue, but as a tool to provide suggestions for effective preventive strategies and personalized, dynamic (from womb to adulthood), systemic, and interdisciplinary healthcare approach.
Panisi Cristina, Guerini Franca Rosa, Abruzzo Provvidenza Maria, Balzola Federico, Biava Pier Mario, Bolotta Alessandra, Brunero Marco, Burgio Ernesto, Chiara Alberto, Clerici Mario, Croce Luigi, Ferreri Carla, Giovannini Niccolò, Ghezzo Alessandro, Grossi Enzo, Keller Roberto, Manzotti Andrea, Marini Marina, Migliore Lucia, Moderato Lucio, Moscone Davide, Mussap Michele, Parmeggiani Antonia, Pasin Valentina, Perotti Monica, Piras Cristina, Saresella Marina, Stoccoro Andrea, Toso Tiziana, Vacca Rosa Anna, Vagni David, Vendemmia Salvatore, Villa Laura, Politi Pierluigi, Fanos Vassilios
Autism Spectrum Disorder (ASD), epigenetics, gut dysbiosis, immune activation, machine learning, metabolomics, mitochondrial impairment, oxidative stress, pathogenesis, prevention