Calcium-Binding Proteins in the Autistic Brain-Potential Links to Symptom Development

• Published in: International journal of developmental neuroscience 2025-02, Vol.85 (1), p.e10412
• Main Authors: Tavares, Élyssa Adriolly Freitas, de Souza, Débora Lopes Silva, da Silva Gomes, Francisca Tayná, Holanda, Maria Vanessa Freitas, Oliveira, Rodrigo Freire, Paiva, Karina Maia, de Gois Morais, Paulo Leonardo Araujo, de Vasconcelos, Cláudio Lopes, de Paiva Cavalcanti, Diogo Manuel Lopes, de Paiva Cavalcanti, José Rodolfo Lopes
• Format: Article
• Language: English
• Subjects: Animals; Autism Spectrum Disorder - metabolism; Autistic Disorder - metabolism; Autistic Disorder - pathology; Brain - metabolism; Calbindin 2 - metabolism; Calbindins - metabolism; Calcium-Binding Proteins - metabolism; Humans; Parvalbumins - metabolism
• ISSN: 0736-5748; 1873-474X; 1873-474X
• DOI: 10.1002/jdn.10412

Autism spectrum disorder (ASD) is a complex challenge, influenced by genetic and environmental factors. This review focuses on the proteins calbindin (CB), calretinin (CR) and parvalbumin (PV) in the context of ASD, exploring their clinical correlations and providing a deeper understanding of the spectrum. In addition, we seek to understand the role of these proteins in GABAergic regulation and their implication in the pathophysiology of ASD. The studies reviewed revealed a significant decrease in PV+ interneurons in the prefrontal cortex of individuals with ASD compared with typical controls. This reduction is associated with local synaptic hyperconnectivity, characterized by an increase in the number of excitatory synapses and a reduction in inhibitory synapses. A correlation was also observed between the decrease in PV+ and the severity of the behavioural symptoms of ASD. The research highlights GABAergic imbalance as a crucial component in the neuropathology of ASD, highlighting the role of calcium-binding proteins, especially PV, in regulating neuronal excitability and modulating synaptic connectivity. These findings provide valuable insights for the development of new therapeutic strategies intended to modulate neuronal activity and improve the symptoms associated with ASD.