The mutation that causes Rett syndrome may spark uncontrolled inflammation throughout the body and brain, suggests a study published last week. The findings may explain the syndrome’s wide range of symptoms, from seizures to gut problems.

An analysis of genes expressed in the postmortem brains of people with autism has identified three molecular pathways linked to the disorder. The findings, published 10 December in Nature Communications, add to mounting evidence that the myriad causes of autism converge on common biological processes.

A new study points to a possible link between inflammation in the womb, brain overgrowth and the behavioral impairments seen in autism.
 

Loss of MeCP2, the Rett syndrome gene, depletes immune cells throughout the bodies of mice, researchers reported yesterday at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

Some cases of autism may result from glitches in immune cells in the blood: This provocative idea stems from a series of unpublished mouse studies presented yesterday at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

Brains from people with autism have more support cells called glia and fewer neurons than do control brains, suggests a study published 10 January in Molecular Autism.

By matching the genes expressed in particular cell types with those linked to a disorder, researchers may be able to identify the cell types implicated in the disorder, they report in a study published 22 January in the Journal of Neuroscience. They use this method to link interneurons and immune cells to autism.

A temporary shortage of microglia — immune cells in the brain that prune unnecessary neural connections — in infancy can have long-lasting effects on brain circuits and behavior, according to a study published in Nature Neuroscience on 2 February.

Bone marrow transplants, which have been shown to arrest symptoms of Rett syndrome in young mice, have little effect on older mice, according to preliminary results presented Monday at the 2013 Society for Neuroscience annual meeting in San Diego. The findings suggest that this approach may not be a viable treatment for those who already have symptoms of the disorder.

Two new studies bolster the emerging idea that microglia, cells that were long dismissed as passive soldiers of the brain’s immune system, are in fact actively involved in shoring up connections between neurons. The unpublished work was presented Sunday at the 2013 Society for Neuroscience annual meeting in San Diego.