Ricerc@Sapienza

Background: Retinal ganglion cells (RGCs) are the nervous retinal elements which connect the visual receptors to the brain forming the nervous visual system. Functional and/or morphological involvement of RGCs occurs in several ocular and neurological disorders and therefore these cells are targeted in neuroprotective strategies.Cytidine 5-diphosphocholine or Citicoline is an endogenous compound that acts in the biosynthesis of phospholipids of cell membranes and increases neurotransmitters' levels in the Central Nervous System.

Abstract: Purpose: to study the neuroprotective effect of oral citicoline (CT) in patients with primary
open-angle glaucoma (POAG). Methods: this study recruits 110 patients with stage IV POAG and
well-controlled intraocular pressure (IOP). Enrollees were randomly allocated in two groups: therapy
group (TG) or control group (CG). Subjects in TG were treated with citicoline 500 mg / die for 4

Purpose: The aim of the study is to detect the effect of the different intravitreal therapies (anti-VEFG drugs and corticosteroids) on the single layer of retinal ganglion cells (GCL) in patients affected by macular edema. Methods: Forty (17 males/23 females) Caucasian patients (40 eyes) affected by macular edema treated with intravitreal injections (anti-VEGF and steroids) are included. Spectralis HRA-OCT device with a specific protocol for the acquisition and evaluation of the GCL layer has been used.

Neuroprotection is an unmet need in eye disorders characterized by retinal ganglion cell (RGC) death, such as prematurity-induced retinal degeneration, glaucoma, and age-related macular degeneration. In all these disorders excitotoxicity is a prominent component of neuronal damage, but clinical data discourage the development of NMDA receptor antagonists as neuroprotectants. Here, we show that activation of mGlu1 metabotropic glutamate receptors largely contributes to excitotoxic degeneration of RGCs.

Duchenne muscular dystrophy (DMD) is a lethal X-linked muscular disease caused by
defective expression of the cytoskeletal protein dystrophin (Dp427). Selected autonomic
and central neurons, including retinal neurons, express Dp427 and/or dystrophin shorter
isoforms. Because of this, DMD patients may also experience different forms of cognitive
impairment, neurological and autonomic disorders, and specific visual defects. DMDrelated
damages to the nervous system are established during development, suggesting

Excitotoxicity is known to modulate the nuclear accumulation, and thus activity state, of histone deacetylases (HDACs) in pyramidal neurons. In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal ischemia, glaucoma, and acute optic nerve injury. Up to now, however, the effects of in vivo excitotoxicity on the different HDACs in retinal ganglion cells (RGCs) have not been thoroughly investigated.