Retinal layers in Parkinson's disease: A meta-analysis of spectral-domain optical coherence tomography studies

Chrysou, A.; Jansonius, Nomdo M.; Laar, Teus van

doi:10.1016/j.parkreldis.2019.04.023

Cited by 106 publications

(85 citation statements)

References 68 publications

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“…On the other hand, one of the main strengths of this study is related to the short disease duration of PD patients. Considering that several studies showed that macular thinning correlates with PD severity (17,19,31,50), our finding of a reduced retinal thickness in early PD patients could suggest the use of this biomarker as a hallmark of brain degeneration. To support our hypothesis, future larger longitudinal studies on progression of retinal thickness along with microvascular abnormalities are surely needed, and it could be interesting to evaluate how fast the changes occur in retinal morphology as compared to in retinal vascularization, and vice versa.…”

Section: Discussionmentioning

confidence: 60%

Retinal Thickness and Microvascular Pattern in Early Parkinson's Disease

et al. 2020

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A thinning of intraretinal layers has been previously described in Parkinson's disease (PD) patients compared to healthy controls (HCs). Few studies evaluated the possible correlation between retinal thickness and retinal microvascularization. Thus, here we assessed the thickness of retinal layers and microvascular pattern in early PD patients and HCs, using, respectively, spectral-domain optical coherence tomography (SD-OCT) and SD-OCT-angiography (SD-OCT-A), and more interestingly, we evaluated a possible correlation between retinal thickness and microvascular pattern. Patients fulfilling criteria for clinically established/clinically probable PD and HCs were enrolled. Exclusion criteria were any ocular, retinal, and systemic disease impairing the visual system. Retinal vascularization was analyzed using SD-OCT-A, and retinal layer thickness was assessed using SD-OCT. Forty-one eyes from 21 PD patients and 33 eyes from 17 HCs were evaluated. Peripapillary retinal nerve fiber layer (RNFL) and macular RNFL, ganglionic cell layer (GCL), inner plexiform layer (IPL), and inner nuclear layer (INL), resulted to be thinner in PD compared to HCs. Among PD patients, a positive correlation between RNFL, GCL, and IPL thickness and microvascular density was found in the foveal region, also adjusting by age, sex, and, especially, hypertension. Such findings were already present in the early stage of disease and were irrespective of dopaminergic treatment. Thus, the retina might be considered a biomarker of PD and could be a useful instrument for onset and disease progression.

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Section: Discussionmentioning

confidence: 60%

Retinal Thickness and Microvascular Pattern in Early Parkinson's Disease

et al. 2020

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“…To date, only one neuroimaging study has evaluated in vivo the relation between retinal thickness and the integrity of brain regions involved in motor manifestations of PD, finding an association between inner retinal atrophy and lower dopamine transporter uptake in substantia nigra 43 . However, the majority of previous OCT studies in PD failed to demonstrate statistically significant results or yielded contradictory findings regarding the link between retinal atrophy and motor disability or disease duration 22 . Given that macular GCIPL atrophy has been reported in de novo PD patients 23 and in prodromal phases of LBD 24 and the lack of its correlation with disease duration or motor manifestations, it may suggest that retinal injury is an early phenomenon of iPD.…”

Section: Discussionmentioning

confidence: 99%

“…Retinal neurodegeneration, neuronal loss, and anomalous α‐synuclein deposits within inner retinal layers are now well‐known pathological features of LBD patients 21 . Several cross‐sectional studies using OCT have demonstrated that, compared to age‐matched controls, PD patients have an atrophy of inner retina that seems to be associated with disease duration and motor disability 22 . More recent publications have shown that the thinning of macular GCIPL in PD is linked to cognitive impairment in de novo patients 23 and to the risk of dementia 18 .…”

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confidence: 99%

Retinal Thickness Predicts the Risk of Cognitive Decline in Parkinson Disease

Murueta‐Goyena

Pino

Galdós

et al. 2020

Annals of Neurology

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Objective This study was undertaken to analyze longitudinal changes of retinal thickness and their predictive value as biomarkers of disease progression in idiopathic Parkinson's disease (iPD). Methods Patients with Lewy body diseases were enrolled and prospectively evaluated at 3 years, including patients with iPD (n = 42), dementia with Lewy bodies (n = 4), E46K‐SNCA mutation carriers (n = 4), and controls (n = 17). All participants underwent Spectralis retinal optical coherence tomography and Montreal Cognitive Assessment, and Unified Parkinson's Disease Rating Scale score was obtained in patients. Macular ganglion cell–inner plexiform layer complex (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) thickness reduction rates were estimated with linear mixed models. Risk ratios were calculated to evaluate the association between baseline GCIPL and pRNFL thicknesses and the risk of subsequent cognitive and motor worsening, using clinically meaningful cutoffs. Results GCIPL thickness in the parafoveal region (1‐ to 3‐mm ring) presented the largest reduction rate. The annualized atrophy rate was 0.63μm in iPD patients and 0.23μm in controls (p < 0.0001). iPD patients with lower parafoveal GCIPL and pRNFL thickness at baseline presented an increased risk of cognitive decline at 3 years (relative risk [RR] = 3.49, 95% confidence interval [CI] = 1.10–11.1, p = 0.03 and RR = 3.28, 95% CI = 1.03–10.45, p = 0.045, respectively). We did not identify significant associations between retinal thickness and motor deterioration. Interpretation Our results provide evidence of the potential use of optical coherence tomography–measured parafoveal GCIPL thickness to monitor neurodegeneration and to predict the risk of cognitive worsening over time in iPD. ANN NEUROL 2021;89:165–176

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“…Among them, the retina has been recently proposed to reflect the PD brain pathology: phosphorylated α-synuclein deposits, similar to Lewy bodies, have been found in the retina of PD patients, whose density correlated with disease severity. 2,3 In addition, PD patients present several visual symptoms, such as reduced amplitudes in b-waves and oscillatory potentials on electroretinograms (ERGs), reduced visual evoked potentials, inner retinal layer thinning by optical coherence tomography (OCT), 4 impaired motion perception, contrast sensitivity, and color discrimination, [5][6][7][8] circadian rhythm dysfunction, 9,10 and melanopsin-containing retinal ganglion cell (mRGC) degeneration. 11 Considering the described similarities between the neurodegenerative process in the retina and brain, it is natural to wonder whether the dopaminergic cells in the retina are involved in the disease as they are in the brain.…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Retinal Cell Loss and Visual Dysfunction in Parkinson Disease

Ortuño‐Lizarán

Sánchez‐Sáez

Lax

et al. 2020

Annals of Neurology

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Objective: Considering the demonstrated implication of the retina in Parkinson disease (PD) pathology and the importance of dopaminergic cells in this tissue, we aimed to analyze the state of the dopaminergic amacrine cells and some of their main postsynaptic neurons in the retina of PD. Methods: Using immunohistochemistry and confocal microscopy, we evaluated morphology, number, and synaptic connections of dopaminergic cells and their postsynaptic cells, AII amacrine and melanopsin-containing retinal ganglion cells, in control and PD eyes from human donors. Results: In PD, dopaminergic amacrine cell number was reduced between 58% and 26% in different retinal regions, involving a decline in the number of synaptic contacts with AII amacrine cells (by 60%) and melanopsin cells (by 35%). Despite losing their main synaptic input, AII cells were not reduced in number, but they showed cellular alterations compromising their adequate function: (1) a loss of mitochondria inside their lobular appendages, which may indicate an energetic failure; and (2) a loss of connexin 36, suggesting alterations in the AII coupling and in visual signal transmission from the rod pathway. Interpretation: The dopaminergic system impairment and the affection of the rod pathway through the AII cells may explain and be partially responsible for the reduced contrast sensitivity or electroretinographic response described in PD. Also, dopamine reduction and the loss of synaptic contacts with melanopsin cells may contribute to the melanopsin retinal ganglion cell loss previously described and to the disturbances in circadian rhythm and sleep reported in PD patients. These data support the idea that the retina reproduces brain neurodegeneration and is highly involved in PD pathology.

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Retinal layers in Parkinson's disease: A meta-analysis of spectral-domain optical coherence tomography studies

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Cited by 106 publications

References 68 publications

Retinal Thickness and Microvascular Pattern in Early Parkinson's Disease

Retinal Thickness and Microvascular Pattern in Early Parkinson's Disease

Retinal Thickness Predicts the Risk of Cognitive Decline in Parkinson Disease

Dopaminergic Retinal Cell Loss and Visual Dysfunction in Parkinson Disease

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