Retinotopic degeneration of the retina and optic tracts in autosomal dominant Alzheimer's disease

Author:

Adhikari Suman1,Qiao Yuchuan2,Singer Maxwell3,Sagare Abhay45,Jiang Xuejuan6,Shi Yonggang2,Ringman John M.5,Kashani Amir H.1ORCID

Affiliation:

1. Wilmer Eye Institute Johns Hopkins University Baltimore Maryland USA

2. Mark and Mary Stevens Neuroimaging and Informatics Institute Keck School of Medicine University of Southern California Los Angeles California USA

3. Department of Ophthalmology Keck School of Medicine, University of Southern California Los Angeles California USA

4. Zilkha Neurogenetics Institute Keck School of Medicine, University of Southern California Los Angeles California USA

5. Department of Neurology Alzheimer's Disease Research Center Keck School of Medicine, University of Southern California Los Angeles California USA

6. Department of Ophthalmology Keck School of Medicine University of Southern California Los Angeles California USA

Abstract

AbstractINTRODUCTIONWe investigated the correlation between retinal thickness and optic tract integrity in subjects with autosomal dominant Alzheimer's disease (ADAD) causing mutations.METHODSRetinal thicknesses and diffusion tensor images (DTI) were obtained using optical coherence tomography and magnetic resonance imaging, respectively. The association between retinal thickness and DTI measures was adjusted for age, sex, retinotopy, and correlation between eyes.RESULTSOptic tract mean diffusivity and axial diffusivity were negatively correlated with retinotopically defined ganglion cell inner plexiform thickness (GCIPL). Fractional anisotropy was negatively correlated with retinotopically defined retinal nerve fiber layer thickness. There was no correlation between outer nuclear layer (ONL) thickness and any DTI measure.DISCUSSIONIn ADAD, GCIPL thickness is significantly associated with retinotopic optic tract DTI measures even in minimally symptomatic subjects. Similar associations were not present with ONL thickness or when ignoring retinotopy. We provide in vivo evidence for optic tract changes resulting from ganglion cell pathology in ADAD.

Funder

National Institutes of Health

Publisher

Wiley

Subject

Psychiatry and Mental health,Cellular and Molecular Neuroscience,Geriatrics and Gerontology,Neurology (clinical),Developmental Neuroscience,Health Policy,Epidemiology

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