Hidden Neural Defect Linking Autism and Parkinson’s Disease

Summary: Researchers at the University of Missouri report that young adults with autism may show early brain changes linked to Parkinson’s disease. Using Dopamine Transporter (DaT) scans—commonly used to evaluate Parkinson’s in older adults—the team detected irregularities in dopamine recycling in some participants, suggesting DaT imaging might serve as an early biomarker decades before motor symptoms appear.

This preliminary work examined DaT binding in the basal ganglia, the brain region central to motor control and cognitive functions. The findings raise important questions about long-term brain health in autistic individuals and point toward the need for larger, age-diverse studies to clarify risk and timing.

Key Facts

  • Unexpected biomarkers: Dopamine transporter abnormalities—typically observed in Parkinson’s diagnosis among older adults—were identified in some young adults with autism.
  • Elevated risk: Prior epidemiological studies indicate people with autism have an increased risk for Parkinson’s disease, estimated at roughly six times the general population.
  • Basal ganglia focus: The study targeted the basal ganglia, where dopamine signaling supports movement and cognition.
  • Dopamine recycling: Abnormalities involve the transporters that reclaim unused dopamine. Impairment of this recycling process is implicated early in Parkinson’s disease.
  • Clinical interpretation: Four nuclear medicine readings of 12 scans produced two clear abnormalities and two equivocal results, underlining the need for broader studies.

Source: University of Missouri

University of Missouri researchers have identified DaT scan abnormalities in some young adults with autism that may help explain their higher lifetime risk of 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

The study focused on dopamine transporters, proteins that remove and recycle dopamine after it is released into synapses. Dopamine supports memory, motivation, attention, behavior and, importantly for Parkinson’s disease, motor function. Disruption of these transporters is an early hallmark of Parkinson’s, which is why DaT imaging is valuable in diagnosis and evaluation of the disease.

David Beversdorf, a professor in the School of Medicine and College of Arts and Science and a clinician at the Thompson Center for Autism and Neurodevelopment, explained that while researchers have previously examined overall dopamine levels in autism, this study looked specifically at transporter function within the basal ganglia. “No one had thought to examine DaT scans in young adults with autism,” he said, adding that these initial observations warrant further investigation.

The research team analyzed DaT SPECT scans from 12 young adults with autism. Four experienced nuclear medicine specialists independently reviewed the images. All reviewers agreed that two participants showed clear abnormalities in striatal DaT uptake, eight were considered normal, and two cases were classified as ambiguous. Although the sample is small, the presence of DaT irregularities in this young group was unexpected given that DaT imaging is usually applied to older adults presenting with parkinsonian symptoms.

The authors emphasize caution in interpreting these results. The study is a pilot investigation designed to identify potential patterns rather than to establish causal relationships or predict clinical outcomes. In exploratory analyses, participants with abnormal DaT binding also showed differences in functional connectivity between the striatum and regions involved in cognitive control, suggesting these transporter changes may relate to broader network alterations.

Beversdorf and colleagues plan to expand the work by scanning a larger, more age-diverse autism cohort. The goal is to determine whether DaT abnormalities progress with age and whether they correlate with later development of Parkinson’s-like symptoms. Early identification of individuals at higher risk could open opportunities for monitoring and, eventually, interventions aimed at slowing or preventing neurodegeneration.

Clinical implications

If confirmed in larger studies, DaT transporter health could serve as an early-warning marker for Parkinson’s disease in people with autism. Detecting transporter dysfunction decades before motor symptoms emerge would allow clinicians to follow at-risk individuals more closely and consider preventive strategies. The research also underscores the importance of investigating how neurodevelopmental conditions intersect with aging-related neurodegenerative processes.

Funding and publication The pilot study, titled “A Preliminary Investigation of Dopamine Transporter Binding Abnormalities in Individuals With Autism Spectrum Disorder,” was published in Autism Research and supported by the School of Medicine’s Translational Research Informing Useful and Meaningful Precision Health (TRIUMPH) grant. The research team includes Nanan Nuraini, Carrina Appling, Bradley J. Ferguson, Amolak Singh, Amanda Moffitt Gunn, Roopa Bhat, Frank Schraml, B. Blair Braden and David Q. Beversdorf.

Key Questions Answered:

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

A: No. Although population studies report an elevated statistical risk—about six times higher—this does not make Parkinson’s inevitable. The current research aims to find early markers so clinicians can monitor brain health and pursue interventions long before symptoms emerge.

Q: Why study dopamine transporters instead of total dopamine levels?

A: Dopamine transporters act like plumbing that moves and reclaims dopamine. Total dopamine measures provide limited information if transporter function is impaired. Transporters often show dysfunction early in Parkinson’s, making them a more sensitive early indicator than overall dopamine quantity.

Q: Do the transporter abnormalities explain immediate behavioral symptoms in autism?

A: Not necessarily. The researchers initially investigated whether repetitive behaviors linked to autism correlated with DaT abnormalities but found no clear relationship. The observed changes appear largely silent with respect to immediate outward behaviors and may instead relate to long-term brain health.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • The journal paper was reviewed in full by staff.
  • Additional contextual information was added by the editorial team.

About this autism and Parkinson’s disease research news

Author: Brian Consiglio
Source: University of Missouri
Contact: Brian Consiglio – University of Missouri
Image credit: Neuroscience News

Original research: Closed access. Title: “A Preliminary Investigation of Dopamine Transporter Binding Abnormalities in Individuals With Autism Spectrum Disorder.” DOI: 10.1002/aur.70144


Abstract

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

Emerging research on aging in autism consistently documents a substantially elevated risk for Parkinson’s disease, estimated up to sixfold. Atypical dopamine signaling has also been reported in autistic individuals and animal models. While antipsychotic medications—approved for treating irritability in autism spectrum disorder—affect dopaminergic systems, no prior studies have examined the striatal Parkinson’s biomarker using DaT SPECT imaging in adults with ASD.

This pilot study evaluated DaT SPECT scans and performed exploratory functional connectivity analyses in 18–24-year-old individuals with autism. Of the 12 participants analyzed, four demonstrated definite or possible abnormalities in striatal DaT uptake. Exploratory comparisons showed the abnormal DaT group had increased striatal connectivity to the paracingulate region relative to the normal DaT group. These preliminary results are tentative and require replication in larger, longitudinal cohorts to assess links with behavior, treatment response, and progression across the lifespan.