Autism and Parkinson’s Share a Hidden Neural Defect

Summary: Young adults with autism are approximately six times more likely to develop Parkinson’s disease later in life, and researchers may have discovered why.The scientists used DaT (Dopamine Transporter) scans—typically reserved for diagnosing older adults with Parkinson’s—on 12 young adults with autism.

They found that some participants already showed significant abnormalities in how their brains recycle dopamine. These findings suggest that dopamine transporter health could serve as an early-warning biomarker, decades before physical symptoms of Parkinson’s appear.

Key Facts

  • Surprising Biomarkers: Abnormalities in dopamine transporters, usually seen in the elderly during Parkinson’s diagnosis, were found in young adults with autism (average study age was not specified but focused on “young adults”).
  • Increased Risk: Prior data shows people with autism have a 6x higher risk of developing Parkinson’s compared to the general population.
  • Basal Ganglia Focus: The study specifically examined the basal ganglia, the brain region responsible for motor control and cognition, where dopamine processing occurs.
  • Dopamine Recycling: The abnormalities involve the molecules responsible for “recycling” unused dopamine. Disruptions here can impair muscle movement and cognitive function.
  • The Clinical Discovery: Nuclear medicine specialists identified clear abnormalities in 2 out of 12 scans, with another two scans deemed “ambiguous,” signaling a strong need for larger age-diverse studies.

Source: University of Missouri

Researchers at the University of Missouri may have uncovered a clue explaining why young adults with autism are roughly six times more likely to develop Parkinson’s disease later in life.

In a recent study, Mizzou researchers found that some young adults with autism show abnormalities in dopamine transporters — tiny molecules in the brain that recycle unused dopamine — on brain scans that are typically used to diagnose older adults with Parkinson’s disease.

This shows neurons.
Preliminary research suggests that abnormalities in dopamine transporters may link neurodevelopmental conditions like autism to a higher risk of late-life neurodegeneration. Credit: Neuroscience News

Future research could help determine whether the health of dopamine transporters could be an early warning sign of Parkinson’s disease developing later in life.

“While the loss of these dopamine transporters can be biomarkers for Parkinson’s disease, no one had ever thought to look at them in the context of young adults with autism, so hopefully this work can help us explore if there is a potential link going forward,” David Beversdorf, a professor in the School of Medicine and College of Arts and Science, said.

“There has been previous work looking into the total amount of dopamine in the brains of people with autism, but we took a new approach by looking at abnormalities in terms of how dopamine is processed in a specific part of the brain called the basal ganglia via these dopamine transporters.”

Dopamine under the spotlight

Dopamine is a neurotransmitter involved in numerous body functions, such as memory, pleasure, motivation, behavior and attention. Of particular interest to Beversdorf, a clinician at the Thompson Center for Autism and Neurodevelopment, is that dopamine also helps control muscle movement as well as cognition.

Beversdorf, who collaborated with lead author Nanan Nuraini on the study, originally wanted to know whether certain repetitive behaviors common in some young adults with autism, such as hand-flapping or rocking back and forth, were linked with abnormalities in dopamine transporters.

While he did not notice patterns in that regard, what he found surprised him.

Beversdorf looked at Dopamine Transporter (DaT) brain scans of 12 young adults with autism.

Four different nuclear medicine specialists examined the scans. All of them agreed that two of the 12 young adults had abnormal dopamine transporters and that eight appeared normal. They disagreed on the remaining two.

“Since these DaT scans are typically used to diagnose or evaluate older adults with Parkinson’s disease, the appearance of abnormalities in some young adults with autism was very surprising, so we should look into this topic more going forward,” Beversdorf said.

“While it’s too early to jump to conclusions, hopefully our work raises awareness about the importance of monitoring the brain health of young adults with autism as they age.”

Next, Beversdorf hopes to study a broader range of people with autism by conducting more DaT scans across different age groups.

“The earlier we can identify those who might be at greater risk for getting Parkinson’s disease down the road, the sooner we can discuss preventative measures, including whether certain medications could potentially slow down the progression of disease,” Beversdorf said.

Funding: The study, “A preliminary investigation of dopamine transporter binding abnormalities in individuals with autism spectrum disorder,” was published in Autism Research and funded by the School of Medicine’s Translational Research Informing Useful and Meaningful Precision Health (TRIUMPH) grant. 

Key Questions Answered:

Q: Does having autism mean I will get Parkinson’s?

A: No. While the risk is statistically higher (roughly 6 times the average), it doesn’t mean a diagnosis is inevitable. This research is about finding “early markers” so that doctors can monitor brain health and potentially intervene long before symptoms start.

Q: Why study “recycling” molecules instead of just dopamine levels?

A: Think of dopamine like water and transporters like the plumbing. You can have plenty of water, but if the plumbing doesn’t recycle and move it correctly, the system fails. These transporters are often the first things to “break” in Parkinson’s, making them a more precise early indicator than total dopamine levels.

Q: What are the symptoms of this link between autism and Parkinson’s?

A: Interestingly, the researchers initially looked for a link between these brain scans and repetitive behaviors (like hand-flapping), but found none. This suggests the neurological changes are “silent” and primarily affect long-term brain health rather than immediate outward behaviors.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • Journal paper reviewed in full.
  • Additional context added by our staff.

About this Autism and Parkinson’s disease research news

Author: Brian Consiglio
Source: University of Missouri
Contact: Brian Consiglio – University of Missouri
Image: The image is credited to Neuroscience News

Original Research: Closed access.
A Preliminary Investigation of Dopamine Transporter Binding Abnormalities in Individuals With Autism Spectrum Disorder” by Nanan Nuraini, Carrina Appling, Bradley J. Ferguson, Amolak Singh, Amanda Moffitt Gunn, Roopa Bhat, Frank Schraml, B. Blair Braden, David Q. Beversdorf. Autism Research
DOI:10.1002/aur.70144


Abstract

A Preliminary Investigation of Dopamine Transporter Binding Abnormalities in Individuals With Autism Spectrum Disorder

In the emerging literature on aging and autism, a consistently replicated finding is a significantly increased risk for Parkinson’s disease (PD), up to six times higher. Also, atypical dopamine activity has been observed in autistic individuals and animal models.

The only FDA-approved medications for ASD are the atypical antipsychotic medications, which inhibit postsynaptic dopaminergic and serotonergic transmission to treat irritability. Studies using resting state functional magnetic resonance imaging (rsfMRI) show disruption in striatal circuits in ASD.

However, no studies have examined the striatal PD biomarker with dopamine transporter (DaT) single photon emission computed tomography (SPECT) imaging in adults with ASD.

In this pilot study, we aimed to evaluate DaT SPECT in 18–24-year-old individuals with ASD and perform a pilot investigation of functional connectivity (FC) between the striatum and other brain areas.

Four of the 12 participants had definite abnormalities or possible abnormalities in striatal DaT uptake. Participants were then separated into abnormal and normal DaT groups.

In the exploratory analysis, the abnormal DaT group showed greater striatal FC to the paracingulate region compared with the normal DaT group. These pilot findings should be cautiously interpreted.

Larger studies are needed to explore their link to behavioral outcomes and potential in predicting treatment responses. Examining how these findings evolve with age is also crucial, given evidence of the heightened risk of PD in ASD.

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