Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (4): 797-799.doi: 10.4103/1673-5374.322454

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Retinal microglial activation in glaucoma: evolution over time in a unilateral ocular hypertension model

José A. Fernández-Albarral, Ana I. Ramírez, Rosa de Hoz, Juan J. Salazar*   

  1. Instituto de Investigaciones Oftalmológicas Ramón Castroviejo, Universidad Complutense de Madrid, Madrid, Spain (Fernández-Albarral JA, Ramírez AI, de Hoz R, Salazar JJ)
    Facultad de Óptica y Optometría, Departamento de Inmunología, Oftalmología y ORL, Universidad Complutense de Madrid, Madrid, Spain (Ramírez AI, de Hoz R, Salazar JJ)
  • Online:2022-04-15 Published:2021-10-18
  • Contact: Juan J. Salazar, PhD, jjsalazar@med.ucm.es.
  • Supported by:
    The present work was supported by the Ophthalmological Network OFTARED (RD16/0008/0005)‚ of the Institute of Health of Carlos III of the Spanish Ministry of Economy (to AIR, RDH, and JJS); Santander- Complutense University of Madrid Research Projects (PR75/18-21560) (to AIR, RNH, and JJS); José A. Fernández-Albarral is currently supported by a Predoctoral Fellowship (FPU17/01023) from the Spanish Ministry of Science, Innovation, and Universities. 

Abstract: Glaucoma is a neurodegenerative chronic pathology, characterized by the loss of retinal ganglion cells (RGC), which leads to an irreversible vision field loss. The increased intraocular pressure (IOP) constitutes its main risk factor. Nowadays, the main treatments for glaucoma are focused on decreasing IOP; nevertheless, the progression of the disease continues, despite IOP control. This fact shows the existence of other factors that could contribute to the advance of glaucomatous neurodegeneration. The early diagnostics, the use of neuroprotective therapies, and knowledge of the pathological processes are the major challenges associated with the management of this disease. Different pathogenic mechanisms have been proposed to be responsible for RGC death, including oxidative stress, mitochondrial dysfunction, glutamate excitotoxicity, and neuroinflammation (Casson et al., 2012)