Reply to Booij, Geurts and Schalbroeck.
This is a clarification letter, not a new study, so it brings no fresh data or clinical steps.
01Research in Context
What this study did
Nuraini et al. (2026) wrote a short reply letter. They did not run a new experiment.
The letter explains their earlier brain-scan data. The scans looked at dopamine transporters in the striatum of autistic adults.
What they found
No new numbers are given. The authors simply restate that the pilot data are early and need more work.
They remind readers that striatal abnormalities were seen in only some adults.
How this fits with other research
The letter is a direct reply to Nuraini et al. (2026) pilot case series. Both papers talk about the same DaT-SPECT scans.
Kunz et al. (1982) guessed that striatal problems might sit behind autism traits. The new scans give the first human evidence for that old idea.
Carvalho Pereira et al. (2018) and Maier et al. (2022) looked at different brain chemicals (GABA) in adults with autism. Their mixed results show that not every chemical pathway is abnormal, so dopamine findings remain useful.
Why it matters
You can relax: this is not a new protocol to learn. It is a reminder that movement, motivation, and attention circuits may differ in some autistic adults. If a client shows low motor drive or late-onset tremor, consider a neurology referral. Keep watching for larger follow-up studies that may link these scans to real-world behavior.
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02At a glance
03Original abstract
Thank you for your interest in our paper. We agree that there are limitations, but would like to clarify a few aspects. First, the presented images were not transverse slices at a single striatal level. Rather, they were composite images of all of the transverse slices. Also, the previous [18F]-FDOPA PET imaging study in autism examined dopamine synthesis in the striatum rather than dopamine transporter integrity in the same age group as our study (Schalbroeck et al. 2021), and in the cited review, the DAT-SPECT studies were all in children (Zürcher et al. 2015; Xiao-Mian et al. 2005; Makkonen et al. 2008, 2011), while the one DAT-PET study that was in our age range quantified differences, revealing changes in the orbitofrontal cortex, without commenting on the pattern of uptake in the striatum (Zürcher et al. 2015; Nakamura et al. 2010). In fact, none of these previous works commented on the pattern of uptake in the striatum, which is a novel aspect of our observation. We raise these issues just for clarification, and completely agree with your call for caution in the interpretation of our findings. While evidence consistently demonstrates elevated risk of Parkinson's disease (PD) (Wallace et al. 2025), it is certainly not as high as one-third of the ASD population. These imaging findings are not the typical appearance of what is observed in PD. We do not yet know what this means. There is clearly a need for further exploration. However, the abnormalities in some of these cases were sufficiently striking that the senior author was called urgently by the nuclear medicine specialist upon his reading of the images to notify him of the abnormalities. This led us to initiate the process of reporting this finding, and seeking consensus readings across four specialists, which led to complete consensus of “abnormal” for two of the cases, and a partial consensus for two more cases. Thus, we felt this initial finding was worth describing, but completely concur regarding the need for further follow-up to understand the implications. This work was supported by MU School of Medicine through the Translational Research Informing Useful and Meaningful Precision Health (TRIUMPH) grant. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
Autism research : official journal of the International Society for Autism Research, 2026 · doi:10.1002/aur.70231