When “abnormal” is the default: the cure frame inside a cerebellum study
A new cerebellum study repeats an old pattern: start with neurotypical as the baseline, call every difference a defect, and aim for restoration
In August 2025, The Cerebellum published “Protein aggregation and synaptic dysfunction in cerebellum of children and adults with idiopathic autism” by S.H. Fatemi, T.D. Folsom, A. Eschenlauer, and T. Chekouo of the Department of Psychiatry at the University of Minnesota Medical School, with Hennepin Healthcare Research Institute and other collaborators. The paper compares postmortem cerebellar tissue from autistic people to neurotypical controls and treats every difference as dysfunction. Protein aggregation. Oxidative stress. Altered synaptic trafficking. In their frame, these aren’t observations. They’re verdicts.
Language is doing as much work here as the lab equipment. “Impairment” tells the reader this is damage, not difference. “Abnormality” says it is deviation, not adaptation. “Restoration” implies a lost state that must be regained. These words travel. They leave the journal and enter grant proposals, clinical guidelines, policy memos. By the time they reach parents, they’ve become “hope” for reversal.
No autistic authorship. No acknowledgement that living decades under sensory assault, restraint, and constant social correction might leave a biological trace. No attempt to separate what’s core to autistic neurology from what’s the residue of harm. These are not oversights; they are design choices. They keep the story clean, the narrative linear: autism is damage, and damage needs fixing.
This is how cure narratives sustain themselves. You start with neurotypical as the baseline. Define any deviation as loss. Present “restoration” as the only acceptable goal. The logic is tight enough to survive peer review because it never steps outside its own frame.
It’s not just the conclusions — it’s the pipeline they feed. Molecular “targets” give biomedical research a market. Pathology-based findings keep tenure committees happy. Review boards expect “burden reduction” as the default outcome. Funders who would never back autistic-led policy work will throw millions at projects that treat autism as a degenerative brain condition.
By design, this type of study erases alternative hypotheses. What if protein aggregation is an adaptation — a structural adjustment to manage a lifetime of sensory load? What if oxidative stress markers reflect a chronic fight-or-flight state, imposed not by autism but by the systems built against it? These questions are not unscientific. They are simply unasked, because they risk a finding that doesn’t point toward a cure.
And the omissions matter. When autistic people aren’t in the room to challenge the premise, “abnormal” stands uncontested. When there’s no methodology to separate innate neurology from the impact of oppression, the two are collapsed into one. When the control group is always neurotypical, difference is pathology by default.
Zoom out, and this paper slots neatly into a decades-long pattern: postmortem studies that treat autistic bodies as broken versions of a standard model. The details change — different brain region, different molecular pathway — but the narrative arc is the same. It starts with a deviation, frames it as a defect, and ends by pointing toward intervention. The only novelty is the specific biochemical scenery along the way.
It is not anti-science to point this out. It is anti-silence. These studies don’t exist in a vacuum; they exist in a policy landscape where autistic services are rationed, where “evidence-based” often means compliance training, where parents are told to invest in early intervention over lifelong supports. In that landscape, every pathology-framed finding is a political object. It shapes what gets funded, what gets denied, and what futures are considered imaginable.
There’s a reason the paper reads like an obituary for a life it never met. The method requires it. You can’t talk about adaptation if you’ve already decided there’s a normal state to restore. You can’t admit the role of environment if the entire grant rests on locating the problem inside the individual. And you can’t co-author with the people you’re pathologizing without risking a different conclusion.
The harm here isn’t hidden in the supplementary tables. It’s in the premise. Decide that autism is reducible to cerebellar protein patterns, and you can measure forever without touching the truth. You can claim objectivity while carrying the same old frame from one study to the next. You can keep the cure narrative fed without ever saying the word “cure.”
This isn’t just a paper about brains. It’s a paper about power — who holds it, who benefits from it, and who is written out of it. Until molecular autism research starts by asking questions that can leave autism intact, the microscope will keep showing only what the frame allows it to see.