PROTECTING THE RETINAL NEURONS FROM GLAUCOMA: LOWERING OCULAR PRESSURE IS NOT ENOUGH

The retina is theater of a number of biochemical reactions allowing, within its layers, the conversion of
light impulses into electrical signals. The axons of the last neuronal elements, the ganglion cells, form the
optic nerve and transfer the signals to the brain. Therefore, an appropriate cellular communication, not
only within the different retinal cells, but also between the retina itself and the other brain structures, is
fundamental. One of the most diffuse pathologies affecting retinal function and communication, which
thus reverberates in the whole visual system, is glaucoma. This insidious disease is characterized by a
progressive optic nerve degeneration and sight loss which may finally lead to irreversible blindness. Nevertheless,
the progressive nature of this pathology offers an opportunity for therapeutic intervention. To
better understand the cellular processes implicated in the development of glaucoma useful to envision
a targeted pharmacological strategy, this manuscript first examines the complex cellular and functional
organization of the retina and subsequently identifies the targets sensitive to neurodegeneration. Within
this context, high ocular pressure represents a key risk factor. However, recent literature findings highlight
the concept that lowering ocular pressure is not enough to prevent/slow down glaucomatous
damage, suggesting the importance of combining the hypotensive treatment with other pharmacological
approaches, such as the use of neuroprotectants. Therefore, this important and more novel aspect is
extensively considered in this review, also emphasizing the idea that the neuroprotective strategy should
be extended to the entire visual system and not restricted to the retina.