Two disorders, one trajectory? Rethinking the divide between autism and Parkinson’s

For decades, neuroscience has maintained a clear distinction between two categories of brain disorders. On one side are neurodevelopmental disorders, which emerge early in life and reflect disruptions in brain maturation. On the other are neurodegenerative diseases, typically associated with aging and characterized by the progressive breakdown of specific neural structures. This division has long structured how we understand brain pathology. However, this once-stable boundary is now being called into question.

Recent clinical data reveal that individuals diagnosed with autism in childhood, due to differences in communication, emotional regulation, or behavior, face a significantly increased risk of developing Parkinson’s disease later in life, a condition traditionally linked to old age. This unexpected co-occurrence challenges our existing models. How can a developmental disorder potentially lay the groundwork for a neurodegenerative one? Is there a shared biological foundation, a latent vulnerability that first manifests as autistic traits and later evolves into motor symptoms?

These questions go beyond mere diagnostic overlap; they compel us to rethink brain trajectories as continuous processes, unfolding from early life into its later stages. In exploring this hypothesis, neuroscience opens the door to a more integrated understanding of the brain, where disorders are not isolated entities but rather successive expressions of deep, enduring imbalances.

What autism and Parkinson’s reveal about the brain’s continuum

At first glance, autism and Parkinson’s disease appear to belong to entirely different clinical worlds, one rooted in childhood development, the other emerging in the twilight years. This distinction is grounded in a powerful temporal intuition: development versus degeneration. Nevertheless, advances in functional neurology and epidemiology are beginning to blur that line.

Biological overlaps between the two conditions are now coming to light. The dopaminergic system, crucial for both motor regulation and social behavior, appears to be a shared area of dysfunction. Similarly, the cerebellum, long underestimated, is increasingly recognized for its roles in cognition and emotion, and shows abnormalities in both disorders. Shared disruptions in REM sleep, often seen as a sensitive marker of neurobiological imbalance, further point to a possible common pathway.

A recent study led by Joseph Firth’s team at the University of California explored whether a diagnosis of autism spectrum disorder (ASD) might be associated with a higher risk of developing Parkinson’s disease. Analyzing a vast clinical dataset of more than 2.6 million cases, including nearly 87,000 individuals with ASD, the researchers found that autistic adults were nearly three times more likely to be diagnosed with Parkinson’s before age 65 compared to the general population. This elevated risk persisted even after adjusting for psychiatric history, medical comorbidities, and medication use.

The findings reinforce the hypothesis of a structural link between early-life neurodevelopmental vulnerabilities and late-onset neurodegenerative processes. Far from being a statistical anomaly, this convergence forces a deeper reconsideration of how we understand pathological brain trajectories.

One particularly striking insight from the study involves sex distribution. While Parkinson’s typically affects men more often than women, this trend reverses within the autistic population. In this context, autistic women exhibited the highest relative risk of developing the disease. This inversion raises compelling questions about the interaction between gender, autism, and neurobiological vulnerability. It also underscores the need for a better understanding of the often-overlooked female presentation of autism and how it unfolds over time.

These epidemiological findings do more than highlight a correlation, they challenge the assumption that neurological profiles identified in childhood remain stable. The notion of a continuous brain trajectory, marked by heightened sensitivity in certain circuits, begins to make sense. It suggests that we move beyond static diagnostic labels and adopt a more dynamic approach, one that views brain vulnerabilities as evolving processes shaped by time, environment, and biological transitions.

In this light, the statistical link between autism and Parkinson’s is not a data anomaly but a signal. It points to a shared, still poorly understood neurobiological substrate, one whose recognition could reshape how we anticipate and manage long-term neurocognitive trajectories.

One system, two expressions: Dopamine’s role in autism and Parkinson’s

To better understand the connection between autism and Parkinson’s, we must consider a key player in brain function: the dopaminergic system. This network of neurons relies on dopamine, a neurotransmitter essential for movement, motivation, and attention. In Parkinson’s disease, it is the gradual degeneration of dopamine-producing neurons in a region known as the substantia nigra that leads to hallmark motor symptoms such as tremors, rigidity, and slowed movement.

This same system appears to be disrupted in autism, though in a different way. Neuroimaging and pharmacological studies reveal that autistic individuals often exhibit altered dopaminergic activity. This may involve reduced dopamine release, diminished receptor sensitivity, or imbalances between the brain regions that depend on this neurotransmitter.

Such dysfunctions are not without consequence. They may create an early and lasting fragility within specific brain circuits. Over time, this fragility could make these networks more susceptible to gradual deterioration. Indeed, certain signs observed in autistic patients, muscle stiffness, repetitive movements, delayed motor initiation, may not be purely behavioral traits, but early expressions of a neurological sensitivity akin to preclinical Parkinsonian symptoms.

The idea of dopaminergic disruption common to both conditions thus supports a broader biological continuity. It strengthens the hypothesis of a shared cerebral terrain, where early alterations have both immediate developmental effects and longer-term neurological consequences.

A new map of brain vulnerability: Moving beyond diagnostic silos

The emerging link between autism spectrum disorder and Parkinson’s disease carries tangible clinical implications, particularly for the long-term monitoring of autistic individuals. If these individuals face a higher risk of early-onset Parkinsonism, as recent evidence suggests, then adapted clinical vigilance becomes crucial. Subtle signs such as changes in fine motor skills, unusual posture, speech disturbances, or sleep abnormalities may be mistakenly attributed to autism. In reality, they could signal the onset of a neurodegenerative process. Early identification would allow for more targeted interventions, at a stage when therapeutic options are broader and potentially more effective.

However, the implications extend far beyond clinical practice. They call into question the very structure of our diagnostic classifications. The conventional dichotomy, developmental disorders confined to childhood and neurodegenerative diseases to aging, is rooted in a linear, compartmentalized view of brain function. Accumulating evidence suggests that the same biological vulnerability can manifest differently depending on age, life context, and environmental influences. In other words, what we’ve treated as separate entities may simply represent different stages along a single trajectory.

This perspective calls for a more flexible and evolving framework, one that focuses not on fixed labels but on the dynamic unfolding of neurological profiles over time. It aligns with the broader movement toward personalized medicine, integrating clinical data, biological markers, brain imaging, and behavioral observations. Such an approach allows us to better grasp atypical brain development not as a static abnormality, but as an alternative mode of organization, one that can transform or deteriorate depending on life stage.

The idea that early neural imbalance could initially affect development and later resurface as a motor disorder forces us to revise our interpretative frameworks. Autism should no longer be viewed solely as a childhood condition, but as a unique expression of brain function marked by long-standing sensitivity to certain imbalances, sensitivities that may remain stable for years but, in some cases, evolve into degenerative vulnerability.

Adopting this longitudinal view of brain trajectories means letting go of diagnostic silos. It becomes more meaningful to speak in terms of individual pathways, integrating cognitive, motor, sensory, and emotional dimensions across the lifespan. This shift in perspective opens the door to more finely tuned interventions, ones that respond to each person’s evolving needs over time.

Ultimately, the convergence between autism and Parkinson’s disease reveals a reality far more complex than our traditional frameworks suggest. Certain neural vulnerabilities can persist, shift, and even transform over time. This insight challenges us to rethink the boundaries between development and degeneration and to see the brain not as a static entity, but as a living, plastic system, continually reshaped by time and experience.

In this light, autism is no longer a fixed condition but a potential marker of long-term neural dynamics, dynamics that urgently require careful scientific exploration, clinical attention, and theoretical openness.

Reference

Yin, W., Reichenberg, A., Schnaider Beeri, M., Levine, S. Z., Ludvigsson, J. F., Figee, M., & Sandin, S. (2025). Risk of Parkinson Disease in Individuals With Autism Spectrum Disorder. JAMA neurology, 10.1001/jamaneurol.2025.1284. Advance online publication.