کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1913294 | 1535107 | 2015 | 5 صفحه PDF | دانلود رایگان |
• Retinal dopaminergic cell loss and α-synuclein aggregation occurs in Parkinson’s disease
• Optical coherence tomography generates high-resolution characterization of the retina
• Individual retinal layers were segmented masked to participant clinical status
• Several retinal layers including ganglion cell layer were thinner in Parkinson’s disease compared to healthy controls
• Outer plexiform layer was significantly thicker in Parkinson’s disease which may correspond to α-synuclein aggregation in the retina
BackgroundParkinson's disease (PD) is a neurodegenerative disorder associated with dopaminergic cell loss and α-synuclein aggregation in Lewy bodies, which has been demonstrated in the retina.MethodsWe performed a spectral-domain optical coherence tomography (OCT) study in patients with PD and healthy controls to measure the peripapillary retinal nerve fiber layer thickness and macular volume. Intra-retinal segmentation was performed to measure the volume of the retinal nerve fiber (RNFL), ganglion cell (GCL), inner plexiform (IPL), inner nuclear (INL), outer plexiform (OPL), and outer nuclear (ONL) layers. Analysis was carried out blinded to the clinical status of study participants.Results101 PD and 46 healthy control eyes were included in the study. In PD patients, peripapillary retinal nerve fiber layer was not significantly thinner (96.95 μm vs 94.42 μm, p = 0.08) but macular volume was (8.58 mm3 vs 8.33 mm3, p = 0.0002). Intra-retinal segmentation showed that PD subjects have reduced GCL, IPL, INL and ONL volumes. In contrast, the OPL volume was significantly increased (0.81 mm3 vs 0.78 mm3 p = 0.0214).ConclusionsThickening of the OPL is a novel finding which may correspond to the localization of α-synuclein in the OPL of PD patients. We hypothesize that the enlargement of the OPL may represent a potential biomarker of α-synuclein aggregation in PD. This may have significant clinical implications.
Journal: Journal of the Neurological Sciences - Volume 355, Issues 1–2, 15 August 2015, Pages 44–48