People with particularly low levels of FMRP, the protein lacking in those with fragile X syndrome, are more likely to also have autism and severe intellectual disability.

Plugging a leaky mitochondrial membrane may help fragile X neurons to mature and function more efficiently.

Mice missing the autism gene NLGN3 have altered social behaviors and brain responses to the hormone oxytocin, both of which improve after treatment with a drug that helps regulate protein production.

Repeating bits of the genome may be responsible for nearly 3 percent of the genetic architecture of autism.

The overproduction of proteins in brain cells called microglia causes social impairments, cognitive deficits and repetitive behavior in male mice, a new study has found.

A new blood test can identify within seven hours whether a person carries the genetic mutation underlying fragile X syndrome.

Some traits of fragile X syndrome may be due to problems with mitochondria, the cell’s energy factories.

New findings hint at why drugs that work in mouse models of fragile X syndrome have not been effective in people.

Watch the complete replay of Mark Bear discussing the latest research on treatments for fragile X syndrome.

Lovastatin, a drug that lowers cholesterol levels, prevents memory and learning problems in a rat model of fragile X syndrome.