The article discusses the abnormal development of brain connectivity in autism, highlighting the fragmented nature of autism research and the need for a unified approach. It defines autism by a "triad" of deficits: impaired social interaction, communication, and restricted interests with repetitive behaviors. The clinical features are detailed, including speech and nonverbal communication impairments, social behaviors, and intense, narrow interests. The article emphasizes the spectrum of phenotypes, from severe autism to milder forms like Asperger syndrome and the Broader Autism Phenotype. The concept of abnormal neural connectivity is explored, suggesting that high local connectivity and low long-range connectivity may contribute to impairments in higher-order cognition, motor coordination, and perceptual abnormalities. Functional magnetic resonance imaging (fMRI) and electroencephalogram (EEG) studies are used to test these theories, showing abnormal activation patterns in specific brain regions during attention tasks. The cerebellum is highlighted as a key site of abnormal connectivity, with hypoplasia and reduced Purkinje cells in autism. Functional MRI studies reveal abnormal activation in the cerebellum during selective attention and motor tasks, correlating with reduced subregion size. The cerebellum's role in cognitive functions such as attention, social behavior, and language is discussed. The article also examines the temporal binding deficit hypothesis, suggesting that underconnectivity between functional brain regions in autism may be reflected in abnormal gamma band activity. The development of neural structure and function in autism is linked to genetic and neuropathological findings, with early brain overgrowth and altered synaptic structure. The role of immune signaling and maternal viral infections during pregnancy is explored, suggesting potential links to autism. Finally, the article concludes by emphasizing the importance of integrating genetic, neuropathological, neuroanatomical, and physiological findings to better understand the mechanisms underlying autism and to develop more effective treatments.The article discusses the abnormal development of brain connectivity in autism, highlighting the fragmented nature of autism research and the need for a unified approach. It defines autism by a "triad" of deficits: impaired social interaction, communication, and restricted interests with repetitive behaviors. The clinical features are detailed, including speech and nonverbal communication impairments, social behaviors, and intense, narrow interests. The article emphasizes the spectrum of phenotypes, from severe autism to milder forms like Asperger syndrome and the Broader Autism Phenotype. The concept of abnormal neural connectivity is explored, suggesting that high local connectivity and low long-range connectivity may contribute to impairments in higher-order cognition, motor coordination, and perceptual abnormalities. Functional magnetic resonance imaging (fMRI) and electroencephalogram (EEG) studies are used to test these theories, showing abnormal activation patterns in specific brain regions during attention tasks. The cerebellum is highlighted as a key site of abnormal connectivity, with hypoplasia and reduced Purkinje cells in autism. Functional MRI studies reveal abnormal activation in the cerebellum during selective attention and motor tasks, correlating with reduced subregion size. The cerebellum's role in cognitive functions such as attention, social behavior, and language is discussed. The article also examines the temporal binding deficit hypothesis, suggesting that underconnectivity between functional brain regions in autism may be reflected in abnormal gamma band activity. The development of neural structure and function in autism is linked to genetic and neuropathological findings, with early brain overgrowth and altered synaptic structure. The role of immune signaling and maternal viral infections during pregnancy is explored, suggesting potential links to autism. Finally, the article concludes by emphasizing the importance of integrating genetic, neuropathological, neuroanatomical, and physiological findings to better understand the mechanisms underlying autism and to develop more effective treatments.