A variety of reasons exist to possibly explain why excellent experimental neuroprotection studies have not been translated to a functional attenuation of a defined progressive retinal disease like glaucoma. A major problem exists in judging the validity of published experimental studies. For example, it is questionable how the various animal models used really relate to any specific ocular disease. There is also a tendency to accept studies as being correct when reported in high profile journals and/or from leading groups. Another issue is that methods used for the administration of neuroprotectants that relate to acceptable side effects, penetration, pharmacokinetics and therapeutic efficacy in successful animal studies might not translate in the same way to the human situation. Also, most animal studies do not demonstrate functional neuroprotection but rather the preservation of biochemical, physiological or morphological alterations caused by a defined insult. It should however be pointed out that clinical proof to reproduce experimental studies in relation to ocular neuroprotection remains largely unexplored because of costs and where investigated may have been faulty.