In the expanding field of autism research, one protein has gained growing attention: reelin. This complex molecule plays a crucial role in the development and connectivity of the brain. Some scientists have linked altered reelin levels to autism spectrum disorder (ASD), fueling hopes of finding a biological “fingerprint” for autism. But while the science is compelling, voices within the autistic community urge caution — warning against oversimplified conclusions and the persistent search for something to “fix.” In this article, we explore what reelin does, what it doesn’t do, and what its prominence says about the broader discourse on autism.
What is reelin, and why does it matter?
Reelin is a protein essential for organizing brain cells during development and supporting the communication between neurons later in life. You could think of it as a GPS system for the brain’s architecture. Several studies have shown that people with autism tend to have lower levels of reelin — both in brain tissue and blood plasma — suggesting that altered reelin signaling might contribute to differences in brain structure and function.
However, the findings are far from consistent. Some children with autism — particularly boys — show extremely high reelin levels in the blood, without any clear link to behavior or severity of symptoms. These inconsistencies suggest that reelin may play a complex, context-dependent role, one that is likely modulated by many other biological and environmental factors.
The genetic angle: RELN and its limitations
Much of the research focuses on the RELN gene, which encodes the reelin protein. Certain variations in this gene have been found slightly more often in autistic individuals. Yet large-scale population studies show that these variations have weak effects at best and are not consistently replicated. In a small subset of cases, rare mutations in RELN significantly disrupt the production of reelin, but even these mutations are not predictive of autism on their own.
Moreover, reelin is part of a much larger signaling pathway that involves other genes such as DAB1, VLDLR, and ApoER2. Some studies suggest that specific gene-gene interactions, especially in certain ethnic populations, may marginally increase autism risk. And even animal studies hint at sex-based differences in how reelin influences synaptic development — possibly explaining part of the gender gap in autism diagnosis. Still, we’re mostly looking at fragments, not foundations.
The critique: what does the autistic community think?
From within the autistic community, reelin research elicits a complex mix of curiosity and concern. Many autistic advocates are wary of reductionist science that seeks to explain autism solely through brain anomalies or genetic “errors.” The fear is that such research reinforces a medical model in which autism is treated as something broken — something to prevent, fix, or eliminate.
“Why do we keep funding studies to detect autism earlier, rather than investing in how to support autistic people now?” This question echoes across neurodivergent blogs, forums, and conferences. There is growing concern that biological research often serves commercial interests — diagnostics, pharmaceuticals, even prenatal screening — more than the lived needs of autistic people.
That said, some within the community see potential value in biological insights — if they’re used responsibly. Understanding individual differences in reelin signaling, for example, could eventually help explain why some autistic people are more sensitive to medication, stress, or overstimulation. But this requires research grounded in ethics, humility, and — crucially — dialogue with those it aims to help.
A tale of two people
Imagine Sam and Elise. Both are autistic. Sam is a 9-year-old boy with sound sensitivity and frequent sensory overload. Tests reveal low reelin levels in his blood. Elise is a 34-year-old woman who thrives on routine and struggles with abrupt changes. Her reelin levels are normal. Both seek calm, understanding, and a life that fits who they are. For neither of them does reelin research offer an answer to the most pressing question:
“How can I live a good life as myself, in a world that often misunderstands me?”
So what do we do with reelin?
Reelin is fascinating. It sheds light on how brains might develop differently in some people. But fascination is not the same as explanation. And explanation is not the same as understanding. The danger is that we mistake biological differences for deficiencies, or that we treat statistical patterns as universal truths.
Autism is not a single disorder with a single cause. It is a multidimensional phenomenon — neurological, psychological, social, cultural. Reelin may be a piece of that puzzle, but it is not the key. And any science that forgets to ask why we seek such keys — and for whom — risks doing more harm than good.
Conclusion: science in service of dignity
Biological research like that on reelin must be held to a high standard — not just scientifically, but ethically. It must avoid pathologizing difference, listen to the voices of those it studies, and resist the pull toward commercial exploitation.
Autistic people are not just research subjects. They are thinkers, artists, workers, partners, and advocates. If science wants to understand autism, it must first recognize its humanity.
The European Autist 