Abstract
PurposeTo evaluate whether treatment with Citicoline in oral solution (OS-Citicoline) would increase visual function, retinal ganglion cells (RGCs) function, and neural conduction along visual pathways (neuroenhancement), and/or induce preservation of RGCs fibers’ loss (neuroprotection) in non-arteritic ischemic optic neuropathy (NAION), a human model of neurodegeneration.MethodsThirty-six patients with NAION and 20 age-matched controls were enrolled. Nineteen NAION patients received 500 mg/day of OS-Citicoline for a 6-month period followed by 3-month of wash-out (NC Group); 17 NAION patients were not treated (NN Group) from baseline to 9 months. In all subjects at baseline, and in NC and NN eyes at 6 and 9 months of follow-up, we assessed Visual Acuity (VA), Pattern Electroretinogram (PERG), Visual Evoked Potentials (VEP), retinal nerve fiber layer thickness (RNFL-T), and Humphrey 24–2 visual field mean deviation (HFA MD). Mean differences were statistically evaluated with ANOVA between Groups, and linear correlations were analysed with Pearson’s test.ResultsAt 6 months, significant differences between groups for all parameters were observed (ANOVA, p<0.01). In NC eyes, VA increased, PERG responses increased, VEP recordings improved and were significantly correlated with increases in HFA MD (p<0.01), and RNFL-T was unmodified or improved. In contrast, in NN eyes, VA, PERG, VEP responses, RNFL-T, and HFA MD were further worsened. Significant differences were still present at 9-month follow-up in the NN Group and after 3 months of OS-Citicoline wash-out in NC eyes.ConclusionsOS-Citicoline treatment induced neuroenhancement (improvement in RGCs function and neural conduction along visual pathways related to improvement of visual field defects) and neuroprotection (unmodified or improved RNFL morphological condition) in a human model of NAION involving fast RGCs degeneration.Trial registrationClinicalTrials.gov NCT03758118.
Highlights
OS-Citicoline treatment induced neuroenhancement and neuroprotection in a human model of non-arteritic ischemic optic neuropathy (NAION) involving fast retinal ganglion cells (RGCs) degeneration
The degeneration of retinal ganglion cells (RGCs) and their fibers which form the optic nerve can be an expression of neurodegenerative phenomena that may occur in the presence of ocular diseases or due to mechanisms of primary or retrograde degeneration in pathologies involving the Central Nervous System (i.e., Alzheimer’s disease, Parkinson’s disease, and demyelinating optic neuritis). [5,6,7,8]
[9] Psychophysics progressively worsens with regard to functional and structural neuronal impairment [10], as described by unrelated retinal dysfunction and impairment of neural conduction along visual pathways [11], reduced Retinal Nerve Fiber Layer (RNFL) thickness assessed by optical coherence tomography (OCT) [12], and flow impairment of retinal and choriocapillaris peripapillary capillaries [13,14]
Summary
Neurodegeneration is a common feature of brain and/or eye diseases characterised by ongoing pathological loss of neuronal structure and function with consequent cell death by apoptosis [1], necrosis [2], or necroptosis. [3,4].The degeneration of retinal ganglion cells (RGCs) and their fibers which form the optic nerve can be an expression of neurodegenerative phenomena that may occur in the presence of ocular diseases (i.e., glaucoma and ischemic optic neuropathy) or due to mechanisms of primary or retrograde degeneration in pathologies involving the Central Nervous System (i.e., Alzheimer’s disease, Parkinson’s disease, and demyelinating optic neuritis). [5,6,7,8].Non-arteritic anterior ischemic optic neuropathy (NAION) is an irreversible, painless, and acute vascular failure of the optic nerve. [9] Psychophysics progressively worsens with regard to functional and structural neuronal impairment [10], as described by unrelated retinal dysfunction and impairment of neural conduction along visual pathways [11], reduced Retinal Nerve Fiber Layer (RNFL) thickness assessed by optical coherence tomography (OCT) [12], and flow impairment of retinal and choriocapillaris peripapillary capillaries [13,14]. The loss of RGCs fibers (assessed by RNFL thickness) has been reported in a period of 1 to 6 months from the acute injury. [15,16] Given these abnormal morpho-functional characteristics, Khalilpour et al [17] have considered NAION a valuable model of neurodegeneration of the retinal structures forming the optic nerve. In the field of vision, neuroprotection, neurorecovery or neuroenhancement, neurorescue, axoprotection, and neurorepair are potential interventions for maintaining RGCs and morpho-functional integrity of their axons after injury
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