Postnatal immune activation causes social deficits in a mouse model of tuberous sclerosis: Role of microglia and clinical implications

Manuel F. López-Aranda, Ishanu Chattopadhya, Gayle M. Boxx, Elizabeth R. Fraley, Tawnie K. Silva, Miou Zhou, Miranda Phan, Isaiah Herrera, Sunrae Talomam Rochelle Mandanas, Karen Bach and Michael Gandal and Daniel H. Geschwind, Genhong Cheng, Andrey Rzhetsky and Stephanie A. White, Alcino J. Silva. Postnatal immune activation causes social deficits in a mouse model of tuberous sclerosis: Role of microglia and clinical implications. Science Advances, vol 7. 38, 2021. DOI:10.1126/sciadv.abf2073

There is growing evidence that prenatal viral infections triggering immune activation contributes to neuropsychiatric disorders, including schizophrenia and autism spectrum disorders

Kids who had severe infections and are genetically predisposed to autism were more likely to develop the condition. So, the genetic factors don’t trigger autism but environmental factors play a significant role. One of the scientists said that childhood infections may be linked to higher instances of depression m, anxiety, schizophrenia.
  • Study links significant childhood infections to developing autism later.
  • In mouse models, mice that had an immune response later were no longer able to recognize familiar faces. This study was replicated with a focus on social interactions and the mice whose immune system was activated had increased difficulty communicating.
  • A different study reinforces the mouse model that tracked 3.6 million hospitalized children shoeing that hospitalizations due to infections during early childhood can predict a future diagnosis of ASD

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