When a Mouse’s Seizure Becomes Our Symptom
A critique of the RT hyperexcitability autism study
Sigh. Another day, another autism study that uses rodents as stand-ins for autistic people. I smell a rat.
The Study in Question
Science Advances (Aug 20, 2025) published a Stanford-led paper by Jang et al. claiming that hyperexcitable neurons in the reticular thalamus drive “autism spectrum disorder behaviors” in mice.
Using Cntnap2 knockout mice — a line long promoted as a genetic autism model — the authors report that epilepsy drugs and chemogenetic switches suppressed abnormal thalamic activity and “rescued” social preference, grooming and hyperactivity.
On paper, it looks like a breakthrough. In practice, it’s another maze of cure framing, animal proxies and autistic erasure.
Mouse Behaviors as Human Deficits
The study equates:
- Increased grooming → repetitive behaviors
- Less chamber preference → social deficits
- Hyperlocomotion → hyperactivity
By collapsing autism into these proxies, autistic life becomes a score sheet of mouse movements. A stim is not a seizure. A grooming event is not a life. But under this model, both become “symptoms to be reversed.”
The Cure Logic Runs Deep
Every experiment is framed in rescue language:
- Z944 drug trial: success means normalized locomotion and restored “social preference”
- Chemogenetic silencing: success means dampened firing in reticular neurons and less grooming
The paper itself says Z944 “restores social preference and reduces excessive grooming” and highlights “therapeutic potential… to alleviate core behavioral abnormalities in ASD.” These words show the value judgment directly — autism behaviors as problems, suppression as cure. This is not neutral neuroscience. It is a value judgment disguised as physiology.
The Epilepsy Connection as Cover
Epilepsy and autism do co-occur. That overlap allows researchers to position anti-seizure drugs as potential autism treatments. The paper cites seizure conditions like Dravet and absence epilepsy as part of its rationale. That linkage invites slippage: from a clear medical harm (seizures) to a way of being (autism).
The authors stop short of calling autism a seizure disorder, but their framing of shared mechanisms invites the slippage once amplified in press coverage. The rhetorical trick is powerful. Treating seizures sounds urgent and ethical. But the study’s real endpoint is not just stopping seizures but erasing autistic-coded behaviors.