Optical Coherence Tomography as Potential Biomarker in Parkinson’s Disease and Alzheimer’s Disease (P5.177)

Abstract

Objective: This study aimed to directly compare optical coherence tomography (OCT) results in Parkinson’s Disease (PD) and Alzheimer’s Disease (AD) to determine if retinal structural changes are disease-specific or representative of a generalized pattern of retinal atrophy associated with neurodegenerative disease. Background: OCT creates a high-resolution, three-dimensional image of the retina. OCT can therefore provide a direct and real-time window into structural changes associated with neurodegenerative processes. Prior OCT studies of patients with PD and AD have found retinal thinning that may be useful as a disease biomarker, but the disease-specificity and underlying mechanisms of these changes are not known. Methods: 13 patients with PD, 8 patients with AD, and 14 age-matched controls were examined using three OCT scans: a peripapillary scan, a macular volume scan, and an Extended Depth Imaging (EDI) macular scan. The scans were then automatically segmented into retinal layers. Subfoveal choroid and peripapillary retinal nerve fiber layer thickness and macula, ganglion cell layer, and photoreceptor layer volume were compared between groups. Results: The average retinal nerve fiber layer thickness was decreased by 8[percnt] in PD patients compared to both controls and AD patients (p=0.002). In the EDI scans, the average choroid thickness was decreased by 20[percnt] in AD patients compared to both controls and PD patients (p=0.04). Both patient groups showed similar trends of reduced macular volumes compared to controls. Conclusions: In PD and AD, different mechanisms of retinal injury may converge on a similar pattern of structural changes. This result points to a need for longitudinal OCT studies to determine stages of retinal deterioration and demonstrate whether OCT is useful in tracking disease progression. In this way, OCT studies may provide insight into the underlying biology of retinal degeneration in neurodegenerative diseases. Study supported by: NIA Grant #5T35AG029795-08 and the Pritzker School of Medicine

Disclosure: Dr. Boeke has nothing to disclose. Dr. Rosen has nothing to disclose. Dr. Mastrianni has received research support from Janssen Pharmaceuticals. Dr. Xie has nothing to disclose. Dr. Bernard had received personal compensation for activities with Novartis. Dr Bernard has received research support from Biogen Idec.