Glaucoma is an age‐related neurodegenerative pathology, characterized by retinal ganglion cells (RGCs) death, which leads to irreversible blindness. Clinical studies have shown that one of the risk factors for glaucoma is high intraocular pressure (IOP). The only therapeutic strategy currently used in this pathology is the reduction of IOP, which does not always reverse neurodegeneration and stop the progression of the disease. However, there is another more important risk factor for glaucoma than IOP, which is aging. It has been observed that aging can increase the vulnerability of the central nervous system to damage. Changes that occur with aging can make RGCs more vulnerable to damage in the glaucomatous neurodegeneration process. The effects of oxidative stress and chronic exposure to light and inflammation mainly cause alterations in the retina due to aging. In glaucomatous neurodegeneration, as in most neurodegenerative diseases, the immune system is involved. Glial cells are immune cells of the retina and optic nerve. When damage occurs, these cells respond quickly, becoming activated, to help restore tissue homeostasis and ensure the immune privilege of nerve tissue. In addition, with aging, a state of chronic parainflammation occurs, leading to the activation of the microglia and release of cytotoxic factors, such as TNF‐α, nitric oxide and other molecules, that which could significantly exacerbate glaucomatous neurodegeneration. One of the main models for raising IOP is the unilateral model of laser‐induced ocular hypertension (OHT). Studies have analysed RGC death and the neuroinflammatory process (focusing on glial cell changes) in this unilateral laser‐induced OHT model in young adult mice. Considering that glaucoma is an age‐related pathology, and that age is the main risk factor, aged in these studies should have been considered a determinate factor. We have used 15‐month‐old mice, which is the beginning point of the aging process of the mice, which is well established from 18 months. In this study, we found morphological signs of microglial activation and changes in the expression of MHCII, CD68 and P2RY12 in the naïve eyes of 15‐month‐old mice (early stage of aging), compared to young naïve adults. On this study we have also analysed the microglial behaviour in response to an increase in IOP in 15‐month‐old mice in a unilateral laser‐induced OHT mouse model of both OHT and contralateral eyes. We also found microglial morphologic alterations and changes in the expression of MHCII, CD68 and P2RY12 in the eyes of 15‐month‐old OHT mice and in the eyes contralateral to them, compared to the eyes of young adult OHT mice and the eyes contralateral to them. In neurodegenerative diseases associated with aging, such as glaucoma, the neuroinflammatory mechanisms induced by microglial cells have an important implication in the development of disease. The use of aging models to analyses the age‐related retinal pathologies could help to improve our understanding of the progression of these pathologies.