Home Health Does autism develop in the womb? A million dollar question

Does autism develop in the womb? A million dollar question

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Autism is a disorder of neuropsychological development that remains largely unexplored despite the rapid increase in the number of patients. Immune disorders, which are now considered to be the cause of many diseases, also play a role in the development of autism. Brain edema and peripheral immune system disorders are commonly observed in autistic people. In addition, immune disorders are accompanied by disturbances in the intestinal microbiota, which is also thought to be involved in the pathogenesis of the disease through the intestinal-brain axis. However, the underlying mechanisms of these immune disorders have yet to be elucidated.

Given the critical stages in the development of immune lesions and the extensive involvement of the immune system in the development of autism, the research team suggested that the common etiology underlies widespread disorders of immune regulation and comes from different types of progenitor cells. The analysis focused on the hematopoietic cells from which immune cells originate, as well as on the yolk sac and aortic-gonad-mesonephros involved in hematopoiesis at the fetal stage. These results look for common ancestor inflammation in the brain and abnormalities in the peripheral immune system. BTBR mice were used as an idiopathic model for autism for this study.

The results of this study

  • HDAC1 has been identified as the etiology of immune disorders by analyzing the unicellular RNA sequence of AGM blood cells in BTBR mice, an animal model of autism.
  • Analysis of unicellular RNA-seq hematopoietic yolk sac cells also identified HDAC1 as the etiology of microglia developmental abnormalities.
  • Regulation of HDAC activity in the fetal stage improved brain inflammation and immune dysregulation in BTBR mice.
  • Changes have been found in the intestinal environment, especially in the immune system, and lead to disturbances in the intestinal microbiota of BTBR mice.

The results of the study

Unicellular RNA of BTBR mice traced the origin of immune disorders to the embryonic stages of the yolk sac and aortic-gonad-mesonephrosis and determined where macrophages (microglia) and peripheral ones differ. Final hematopoiesis has successfully identified pathological mechanisms at the molecular level within rare progenitor cells in the early stages of development. That is, a common mechanism for regulating transcription via HDAC1, the histone deacetylase that underlies these pathologies, has been found.

We have also shown that manipulation of epigenetic mechanisms at certain stages of development can restore immune disorders in the brain and peripheral tissues. That is, HDAC1 histone deacetylase has been identified as a common mechanism. Administration of inhibitors of this histone (sodium butyrate or romidepsin) at the fetal stage in BTBR mice suppressed elevated levels of inflammatory cytokines and microglia activation.

In addition, impaired immune regulation may determine intestinal dysbacteriosis-specific profiles in autistic model mice, making potential Treg biomarkers and intestinal dysbacteriosis a means of classifying subtypes of immunoregulated autism spectrum disorders.

From the above it is clear that abnormalities in the brain and peripheral organs (such as the gut) observed in autism are caused by epigenetic abnormalities in the hematopoietic stem cell line, the ancestor of immune cells.

Source: Medindia

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