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    Detecting Parkinson With Macular OCT


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    Researchers are getting closer to a future in which Parkinson disease may be detected years before clinical presentation of the debilitating degen­erative condition. University College London (UCL) scientists and colleagues leveraged artificial intelligence and imaging technologies and two large pa­tient databases to discover that people with Parkinson disease have reduced thickness of the ganglion cell-inner plexiform layer (GCIPL) and the inner nuclear layer (INL).1

    “We have known for some time that retinal manifestations of neurodegen­eration can present several years before diagnosis,” said lead study author Siegfried Karl Wagner, MSc, MD, at the Institute of Ophthalmology at UCL. But involvement of these layers sev­eral years before clinical presentation highlights a potential role for retinal imaging in early detection.

    An optical coherence tomography scan shows the nasal macula.

    REDUCED THICKNESS. Optical coherence tomography scan of the nasal macula.

    Cross-sectional analysis. Previous studies—on cadavers, for example—have shown disease-related neurodegen­eration and other abnormalities in the retina of patients with Parkinson disease, but the UCL investigators conducted a cross-sectional analysis to explore whether imaging of the retina can de­tect disease before a clinical diagnosis.

    To detect retinal markers in preva­lent Parkinson disease, they used data from AlzEye, a retrospective cohort of 154,830 patients aged 40 and up who were seen at secondary care ophthalmic hospitals in Lon­don between 2008 and 2018. To evaluate retinal markers in incident Parkinson, they used OCT measurements of the retina from the UK Biobank, a prospective popu­lation-based cohort of 67,311 volunteers aged 40 to 69 who were recruited between 2006 and 2010. Macular retinal nerve fiber layer (mRNFL), GCIPL, and INL thicknesses were extracted from fovea-centered OCT.

    Thin retinal sublayers. Within the AlzEye group, 700 people were found to have prevalent Parkinson disease. These individuals also had thinner GCIPL and INL. Fifty-three people from the UK Biobank developed Parkinson dis­ease and thin GCIPL and INL were also associated with incident Parkinson. Dr. Wagner said he was particularly struck by the fact that the researchers were able to find evidence of degeneration in a separate sublayer of the retina—the INL. He said typically, this is unaffected by other neurological diseases.

    “Interestingly, the inner nuclear layer is one of the major sites of dopa­minergic activity of the retina, the very process that is impaired in Parkinson disease so we could be seeing a primary dopaminergic-related degeneration occurring within the retina. However, it will require further work to confirm this,” he said, noting that other research using UK Biobank data “has shown that reduced inner retinal sublayer thick­nesses can be associated with cognitive decline and the development of Alzhei­mer disease.”

    Uncovering clues to future disease. Dr. Wagner said the study underscores how technology can directly influence medical breakthroughs—that artificial intelligence machine learning com­bined with high-resolution ophthalmic imaging techniques means “we can pick up much subtler signs of disease” earlier than ever before. He said it is exciting that this technology can glean quantitative data from retinal scans with high precision.

    “It’s important to emphasize that we found group-level differences in our report. Translating this to individual level prediction and establishing bio­markers for neurodegenerative disease will take considerable additional work,” Dr. Wagner said. And many of these in­dices vary significantly throughout the normal population and are intimately associated with other key variables, from refractive error to age.

    What’s more, he said, “Quality control of retinal imaging and measure­ment error remains a crucial obstacle to implementing any of these findings for prognostic benefit.”

    In the larger context, Dr. Wagner estimates it could take more than three years before this kind of testing for markers of Parkinson disease will come to the clinic.

    —Brian Mastroianni


    1 Wagner SK et al. Neurology. Published online Aug. 21, 2023.


    Relevant financial disclosures: Dr. Wagner—None.

    For full disclosures and the disclosure key, see below.

    Full Financial Disclosures

    Dr. Wagner—None.

    Dr. Ramulu—Heru: C; Aerie Pharmaceuticals: C; Ivantis: C; Implandata: C; W.L. Gore: C.

    Dr. Almidani—None.

    Dr. Palestine—Tarsier Pharma: C.

    Ms. Rajeswaren—None.

    Dr. Shields—Aura Biosciences: C; Ideaya Biosciences: C; Immunocore: C; iOnctura: C.

    Disclosure Category



    Consultant/Advisor C Consultant fee, paid advisory boards, or fees for attending a meeting.
    Employee E Hired to work for compensation or received a W2 from a company.
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    Independent contractor I Contracted work, including contracted research.
    Lecture fees/Speakers bureau L Lecture fees or honoraria, travel fees or reimbursements when speaking at the invitation of a commercial company.
    Patents/Royalty P Beneficiary of patents and/or royalties for intellectual property.
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    Grant support S Grant support or other financial support from all sources, including research support from government agencies (e.g., NIH), foundations, device manufacturers, and\or pharmaceutical companies. Research funding should be disclosed by the principal or named investigator even if your institution receives the grant and manages the funds.
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