Inadequate Myelination of Neurons Tied to Autism: Study

A mouse model of autism and postmortem brains of autistic individuals showed a lack of mature oligodendrocytes and less myelination than controls.

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Insufficient myelination, likely caused by a lack of mature oligodendrocytes, is linked to autism spectrum disorder, according to a study in mice and postmortem human brains published yesterday (February 3) in Nature Neuroscience.

Myelin, the fatty substance that sheaths and insulates the axons of neurons, is responsible for aiding the quick delivery of signals throughout the brain. Too little myelin leaves the cells vulnerable to damage (as with multiple sclerosis), while too much can muddle the message. Oligodendrocytes (OL) are the cells that control myelination. Previous research has shown that myelin is typically thinner in those with autism spectrum disorder (ASD), while the current study explores the source of the problem.

While studying mouse brains for genetic mutations that cause Pitt-Hopkins syndrome, an autism-related genetic disorder, the team noticed irregular myelination and inconsistent expression of Tcf4, a gene that regulates OL activity.

Turning their attention to ...

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Meet the Author

  • Lisa Winter

    Lisa Winter became social media editor for The Scientist in 2017. In addition to her duties on social media platforms, she also pens obituaries for the website. She graduated from Arizona State University, where she studied genetics, cell, and developmental biology.
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