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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.

Written byLisa Winter
| 2 min read

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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.

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Meet the Author

  • Lisa joined The Scientist in 2017. As social media editor, some of her duties include creating content, managing interactions, and developing strategies for the brand’s social media presence. She also contributes to the News & Opinion section of the website. Lisa holds a degree in Biological Sciences with a concentration in genetics, cell, and developmental biology from Arizona State University and has worked in science communication since 2012.

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