Autism or it starts in the womb?

Molecular Psychiatry [IF:1992] ① Single-cell RNA sequencing in a mouse model of idiopathic autism identified HDAC1 as the cause of immune abnormalities;② HDAC1-mediated epigenetic mechanisms are dysregulated in aorta-gonad-mesonephros and yolk sac progenitor cells It can alter the hematopoietic function during embryogenesis and down-regulate the expression of AP-1 complexes in the developing microglia;③ These changes lead to dysregulation of the immune system, resulting in disturbance of the intestinal flora and hyperactivity of microglia in the brain;④ In fetuses Periodically modulating HDAC activity can improve brain inflammation and immune dysregulation in BTBR mice; ⑤Immune dysregulation is associated with specific microbiota composition, or may serve as a biomarker for identifying immune dysregulation subtypes of auti. A common epigenetic mechanism across different cellular origins underlies systemic immune dysregulation in an idiopathic autism mouse model 05-02, doi: 11038/s41380-022-01566-yIt is now thought to play an important role in the development of auti. Studies have found that people with autism are often accompanied by brain inflammation and peripheral immune system abnormalities, and immune abnormalities are also accompanied by intestinal flora dysbios. Recently, a team from the Institute of Physics and Chemistry in Japan published a new study in Molecular Psychiatry, which found that idiopathic autism is caused by epigenetic abnormalities in hematopoietic cells during fetal development, and immune dysregulation is also associated with specific microbiota compositi. relat. In conclusion, this study provides a new direction for solving the systemic immune dysregulation of autism patients, and provides new insights into the future precision treatment of auti.   Disclaimer: This article only represents the author's personal opinion and has nothing to do with China Probiotics Netwo. Its originality and the text and content stated in the text have not been verified by this site, and this site does not make any guarantee or commitment to the authenticity, completeness and timeliness of this text and all or part of its content and te. Readers are only for reference and please Verify the relevant content yourse. Copyright Notice Some articles reproduced on this site are not original, and their copyright and responsibility belong to the original auth. All reprinted articles, links and pictures on this website are for the purpose of conveying more information, and the source and author are clearly indicat. Media or individuals who do not wish to be reprinted can contact us for infringing information that can provide sufficient eviden. , bio149 will be deleted within 12 hours after confirmati. Users are welcome to submit original articles to 86371366@. com, which will be published on the homepage after review, and the copyright and responsibility of the articles belong to the send.

Molecular Psychiatry① Single-cell RNA sequencing in a mouse model of idiopathic autism identified HDAC1 as the cause of immune abnormalities;② HDAC1-mediated epigenetic mechanisms are dysregulated in aorta-gonad-mesonephros and yolk sac progenitor cells It can alter the hematopoietic function during embryogenesis and down-regulate the expression of AP-1 complexes in the developing microglia;③ These changes lead to dysregulation of the immune system, resulting in disturbance of the intestinal flora and hyperactivity of microglia in the brain;④ In fetuses Periodically modulating HDAC activity can improve brain inflammation and immune dysregulation in BTBR mice; ⑤Immune dysregulation is associated with specific microbiota composition, or may serve as a biomarker for identifying immune dysregulation subtypes of auti.
A common epigenetic mechanism across different cellular origins underlies systemic immune dysregulation in an idiopathic autism mouse model 05-02, doi: 11038/s41380-022-01566-yIt is now thought to play an important role in the development of auti.

Studies have found that people with autism are often accompanied by brain inflammation and peripheral immune system abnormalities, and immune abnormalities are also accompanied by intestinal flora dysbios.

Recently, a team from the Institute of Physics and Chemistry in Japan published a new study in Molecular Psychiatry, which found that idiopathic autism is caused by epigenetic abnormalities in hematopoietic cells during fetal development, and immune dysregulation is also associated with specific microbiota compositi.

relat.

In conclusion, this study provides a new direction for solving the systemic immune dysregulation of autism patients, and provides new insights into the future precision treatment of auti.

---

Molecular Psychiatry① Single-cell RNA sequencing in a mouse model of idiopathic autism identified HDAC1 as the cause of immune abnormalities;② HDAC1-mediated epigenetic mechanisms are dysregulated in aorta-gonad-mesonephros and yolk sac progenitor cells It can alter the hematopoietic function during embryogenesis and down-regulate the expression of AP-1 complexes in the developing microglia;③ These changes lead to dysregulation of the immune system, resulting in disturbance of the intestinal flora and hyperactivity of microglia in the brain;④ In fetuses Periodically modulating HDAC activity can improve brain inflammation and immune dysregulation in BTBR mice; ⑤Immune dysregulation is associated with specific microbiota composition, or may serve as a biomarker for identifying immune dysregulation subtypes of auti.

A common epigenetic mechanism across different cellular origins underlies systemic immune dysregulation in an idiopathic autism mouse model 05-02, doi: 11038/s41380-022-01566-yIt is now thought to play an important role in the development of auti.

Studies have found that people with autism are often accompanied by brain inflammation and peripheral immune system abnormalities, and immune abnormalities are also accompanied by intestinal flora dysbios.

Recently, a team from the Institute of Physics and Chemistry in Japan published a new study in Molecular Psychiatry, which found that idiopathic autism is caused by epigenetic abnormalities in hematopoietic cells during fetal development, and immune dysregulation is also associated with specific microbiota compositi.

relat.

In conclusion, this study provides a new direction for solving the systemic immune dysregulation of autism patients, and provides new insights into the future precision treatment of auti.

---

Molecular Psychiatry[IF:1992]① Single-cell RNA sequencing in a mouse model of idiopathic autism identified HDAC1 as the cause of immune abnormalities;② In aortic-gonad-mesonephros and yolk sac progenitor cells, HDAC1-mediated Dysregulation of epigenetic mechanisms alters hematopoiesis during embryogenesis and downregulates AP-1 complex expression in developing microglia;③ These changes lead to dysregulation of the immune system, resulting in disturbance of the gut microbiota and excess of microglia in the brain ④ Modulation of HDAC activityduring fetal period ameliorates brain inflammation and immune dysregulation in BTBR mice; ⑤ Immune dysregulation is associated with specific microbiota composition, or may serve as a biomarker for identifying immune dysregulated subtypes of auti.

A common epigenetic mechanism across different cellular origins underlies systemic immune dysregulation in an idiopathic autism mouse model 05-02, doi: 11038/s41380-022-01566-yIt is now thought to play an important role in the development of auti.

Studies have found that people with autism are often accompanied by brain inflammation and peripheral immune system abnormalities, and immune abnormalities are also accompanied by intestinal flora dysbios.

Recently, a team from the Institute of Physics and Chemistry in Japan published a new study in Molecular Psychiatry, which found that idiopathic autism is caused by epigenetic abnormalities in hematopoietic cells during fetal development, and immune dysregulation is also associated with specific microbiota compositi.

relat.

In conclusion, this study provides a new direction for solving the systemic immune dysregulation of autism patients, and provides new insights into the future precision treatment of auti.

---