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Fragile X study uncovers brainwave biomarker bridging humans and mice
Researchers discover shared low-frequency brainwave patterns in fragile X syndrome that could aid treatment development
Published on Feb. 11, 2026
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A collaboration centered at MIT discovered that mice modeling the autism spectrum disorder fragile X syndrome exhibit the same pattern of differences in low-frequency waves as human patients. The novel approach used for analysis enabled the researchers to uncover specific and robust patterns of differences in low-frequency brainwaves between typical and fragile X brains shared between species at each age range. The researchers were also able to relate the brainwaves to specific inhibitory neural activity in the mice and show that the biomarker was able to indicate the effects of even single doses of a candidate treatment for fragile X called arbaclofen.
Why it matters
Numerous potential treatments for neurological conditions, including autism spectrum disorders, have worked well in lab mice but then disappointed in humans. Having a non-invasive, objective readout of treatment efficacy that is shared in both species could help advance treatment studies and bridge the gap between animal and human research.
The details
The researchers measured EEG over the occipital lobe of humans and on the surface of the visual cortex of the mice, measuring power across the frequency spectrum. They found that in adult men and mice alike, a peak in the power of low frequency waves is shifted to a significantly slower frequency in fragile X cases compared to in neurotypical cases. Meanwhile, in fragile X boys and juvenile mice, while the peak is somewhat shifted to a slower frequency, what is really significant is a reduced power in that same peak. The researchers were able to identify that the peak in question is actually made of two distinct subpeaks and that the lower frequency subpeak is the one that varies specifically with fragile X syndrome. Experiments manipulating somatostatin interneurons specifically affected the lower-frequency subpeak that contained the newly discovered biomarker in fragile X model mice.
- The study was published on February 11, 2026.
The players
Sara Kornfeld-Sylla
A postdoc who led the research and earned her PhD in Mark Bear's lab in 2024, continuing the research as a FRAXA postdoctoral fellow.
Mark Bear
A Picower Professor at MIT and a faculty member in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences.
Boston Children's Hospital
Collaborated with the researchers by gathering and sharing data for the study.
Phelan-McDermid Syndrome Foundation
Collaborated with the researchers by gathering and sharing data for the study.
Cincinnati Children's Hospital
Collaborated with the researchers by gathering and sharing data for the study.
What they’re saying
“This research weaves together these different datasets and finds the connection between the brainwave activity that's happening in fragile X humans that is different from typically developed humans and in the fragile X mouse model that is different than the 'wild-type' mice.”
— Sara Kornfeld-Sylla, Postdoc
“Because that is something we can measure in mice and humans minimally invasively, you can pose the question: if drug treatment X affects this signature in the mouse, at what dose does that same drug treatment change that same signature in a human?”
— Mark Bear, Picower Professor, MIT
What’s next
The researchers plan to further investigate the relationship between the brainwave biomarker and the underlying neural activity in fragile X syndrome, as well as explore the potential for using the biomarker to guide the development and testing of new treatments.
The takeaway
The discovery of a shared brainwave biomarker between fragile X patients and mouse models of the disorder represents an important step forward in bridging the gap between animal and human research, which could ultimately accelerate the development of more effective treatments for this and potentially other neurological conditions.
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