Related Experiment Video
Updated: May 15, 2026
In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
Published on: May 11, 2015
Serum Glial Fibrillary Acidic Protein and Retinal Neuronal Loss as Additive Prognostic Markers of Disability in
Shaumiya Sellathurai1,2,3,4,5, Kean Schoenholzer1,2,3,4,5, Federico Burguet Villena1,2,3,4,5
1Department of Neurology, University Hospital Basel, Switzerland.
Background And Objectives:
In people with multiple sclerosis (pwMS), optical coherence tomography (OCT) quantifies loss of neurons (macular ganglion cell-inner plexiform layer [mGCIPL]) and axons (peripapillary retinal nerve fiber layer [pRNFL]) in the retina. Serum glial fibrillary acidic protein (sGFAP) is a promising astrocytic biomarker to capture disease progression in pwMS. We aimed to investigate the relationship between OCT markers and sGFAP in pwMS and explore their additive value in predicting disability progression.
Methods:
PwMS and healthy controls underwent OCT at baseline (BL), excluding eyes with inter-eye asymmetry. Age, sex, and body mass index-adjusted Z scores of sGFAP were calculated. Cross-sectional and longitudinal associations between sGFAP and retinal layers were estimated using linear regression- and mixed-effects models (LMM). The additive effect of BL-OCT and BL-sGFAP on the trajectory of the Expanded Disability Status Scale (EDSS) was estimated using LMM, whereby pwMS were stratified into: group (1): low sGFAP Z score (<3rd quartile,
Results:
Two hundred and sixty-one pwMS (mean age: 48 years (y), female: 63%, on disease-modifying treatment: 80%, mean thickness of pRNFL: 94 μm and mGCIPL: 66 μm) and 52 controls (age: 52 years, female: 65%, pRNFL: 101 μm, mGCIPL: 72 μm) were included. At BL, pRNFL (β = -0.01, p = 0.042) and mGCIPL (β = -0.02, p = 0.013) were negatively associated with sGFAP Z scores in pwMS, but not in controls (p = 0.950, p = 0.386). BL-mGCIPL was also associated with sGFAP trajectories (β = -0.003, p = 0.044), over a median follow-up of 2.9 years. Compared with pwMS with good results in both markers (group 1), those with either high sGFAP or thin mGCIPL had a steeper EDSS increase (β = 0.030, p = 0.048), while pwMS with both high sGFAP and thin mGCIPL (group 3) showed the steepest trajectory of the EDSS (β = 0.101, p < 0.001).
Discussion:
Our findings show a close relationship between astrocytic activation/injury and neurodegeneration in the CNS, measured at the retinal level. Moreover, they highlight an additive role of mGCIPL and sGFAP for identification of pwMS at higher risk of disability worsening.
