Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons.
Qiong Xu, Yuan-Yuan Liu, Xiaoming Wang and 8 others
PMID 30574290WHAT IT FOUND
CHD8 deficiency slowed axon and dendrite growth and delayed cortical neuron migration in mouse and cell models.
This is a molecular mechanism in autism-related CHD8 mutations, not a therapy finding.
Key findings
01In cultured mouse cortical neurons, lowering CHD8 decreased total axon growth, and adding human CHD8 rescued the axon length defect.
02In mouse cortex after in utero electroporation, Chd8 shRNA#2 retarded callosal axon growth, and human CHD8 rescued the phenotype.
03Chd8 knockdown delayed radial migration of cortical neurons at an embryonic time point, but migration was comparable by postnatal days 3 and 7.
STILL TO COME
How it was doneWhat they found
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What it does not show
This is a basic mechanism study in mouse and cell systems, not a clinical trial in people with autism or CHD8 mutations. The human data were from a postmortem brain sample from a 6-year-old child, so they cannot show what CHD8 does across ages or in living patients. The experiments measured axon growth, dendrite growth, and neuron migration, not communication, behavior, or therapy response. The migration delay was seen at E18.5 and was not present by P3 and P7, so it does not show a lasting structural change. Different studies of Chd8 disruption report opposite or inconsistent findings, so one mouse model may not match human CHD8-related autism.
Declared interests
The work was supported by the National Science Foundation of China, the National Natural Science Foundation of China, the Science and Technology Commission of Shanghai Municipality, and the National Institutes of Health. The supplied text does not report commercial funding or author conflicts of interest.
The easy way to misread this
Do not read this as evidence that CHD8 deficiency causes autism symptoms in patients or that any therapy should change. The work was done in cultured mouse neurons and mouse brain development, with a human brain sample, and it measured axon growth, dendrite growth, and neuron migration, not communication or behavior.