080210xf's Blog

L'X fragile sera vaincu | Fragile X will be conquered

From kittens to Fragile X: Do all autisms share a common thread?

Researchers at Children’s Hospital Boston and the Massachusetts Institute of Technology collaborate to learn more about the neurological underpinnings of autism.

By Mustafa Sahin |

Mark Bear’s research interests have taken him from studying vision in kittens to learning and memory in mouse models, and more recently, to the study of Fragile X syndrome, one of the leading genetic causes of autism and intellectual disability in humans.

Along the way, he has made several ground-breaking contributions to neuroscience – one of which he described as one of MIT’s presenters at this week’s inaugural CHB-MIT Research Enterprise Symposium, which kicked off an exciting new scientific collaboration between MIT and Children’s.

I have followed Mark Bear’s work since I was an undergraduate at Brown University, where he used to teach the Introduction to Neuroscience course.

That’s where I first learned about the seminal experiments in kittens (see this PDF), showing that covering one eye at birth rewires their brains not to “see” out of that eye, work that Bear was continuing to refine. Our paths crossed again more recently due to our common interest in studying autism. While his lab was working on Fragile X syndrome, my lab has focused on understanding brain wiring abnormalities in another genetic cause of autism, Tuberous Sclerosis Complex.

Bear has discovered a particular way that the brain rewires and changes its configuration of synapses, or points of connection between neurons, in response to experience. Just like cars, synapses need both a gas pedal and a brake. The gas pedal is the strengthening (potentiation) of the synapse, while the brake is weakening (depression) of the synapse. If either the gas pedal or the brake is not working, the synapse doesn’t function properly. Together, these faulty synapses cause the larger neural circuit to function abnormally.

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