People with Parkinson’s disease had retinal changes that could be seen with optical coherence tomography (OCT) years before diagnosis, cross-sectional data suggested.

Both incident and prevalent Parkinson’s disease were associated with reduced ganglion cell-inner plexiform layer (GCIPL) and inner nuclear layer (INL) thicknesses, reported Siegfried Karl Wagner, MSc, MD, of University College London in England, and co-authors.

People with prevalent Parkinson’s disease had thinner GCIPL (-2.12 μm, P=8.2 × 10^-5) and INL (-0.99 μm, P=2.1 × 10-⁴) after adjusting for age, sex, ethnicity, hypertension, and diabetes, the researchers wrote in Neurology.

Incident Parkinson’s also was associated with thinner GCIPL (HR 0.62 per standard deviation increase, P=0.002) and thinner INL (HR 0.70, P=0.026).

The study “sets new standards for the role of retinal morphology as potential biomarker in neurodegenerative disease,” observed Valeria Koska and Philipp Albrecht, MD, both of Heinrich Heine University Düsseldorf in Germany, in an accompanying editorial.

“It not only corroborates previous studies but also provides new evidence, e.g., a reduced thickness of the inner nuclear layer,” Koska and Albrecht wrote. “It fosters our understanding that [Parkinson’s] is a systemic disease, which extends beyond dopaminergic neurons and also involves the retina as peripheral part of the central nervous system already at a very early and apparently even presymptomatic stage.”

The effect sizes in the study were small and the practical value of using retinal OCT images to identify early Parkinson’s with the current protocols and technology in clinical care is limited, the editorialists noted.

“However, with the advent of artificial intelligence, they might prove useful for the development of new multivariable prognostic factors based on combinations of several biomarkers,” they pointed out.

In previous studies, retinal OCT has shown promise as a diagnostic aid for mild cognitive impairment and has been studied as a potential biomarker of presymptomatic Alzheimer’s disease.

Wagner and co-authors evaluated prevalent Parkinson’s disease among people in the retrospective AlzEye cohort in England and incident disease in the prospective U.K. Biobank cohort.

In the AlzEye cohort, 700 individuals had prevalent Parkinson’s disease and 105,770 people were controls. Mean age was about 66 and 51.7% were women. The U.K. Biobank study included 50,405 participants with a mean age of 56 and 54.7% were women. In this cohort, 53 people developed Parkinson’s disease over an average of 7.3 years.

All participants had non-mydriatic macula-centered OCT imaging. In the U.K. Biobank cohort, researchers included only participants who had retinal imaging at their initial assessment visit (baseline). U.K. Biobank participants who self-reported Parkinson’s disease at baseline were excluded from the study.

Parkinson’s disease was defined by diagnostic codes. People with diagnostic codes for all-cause dementia were excluded.

In the AlzEye group, people with Parkinson’s were older and more likely to be male, hypertensive, and have diabetes. In the U.K. Biobank cohort, adjusted survival analysis showed that age and male sex were associated with incident Parkinson’s disease.

In the U.K. Biobank group, the association between thinner GCIPL or INL and incident Parkinson’s disease persisted even when participants diagnosed with Parkinson’s in the first 24 months after retinal imaging were excluded.

The study had several limitations, Wagner and colleagues acknowledged. The AlzEye cohort did not have detailed clinical information about Parkinson’s status, and retinal changes could not be related to disease duration or severity. Because Parkinson’s disease was identified by diagnostic codes, some cases may have been missed.

Future studies are needed to determine whether the progression of GCIPL atrophy is driven by Parkinson’s brain changes or whether INL thinning precedes GCIPL atrophy, the researchers added.

“I continue to be amazed by what we can discover through eye scans,” Wagner said in a statement. “While we are not yet ready to predict whether an individual will develop Parkinson’s, we hope that this method could soon become a pre-screening tool for people at risk of disease.”

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