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Editors Selection IGR 9-1

Medical treatment: Brimonidine neuroprotection

Comment by Michal Schwartz on:

16813 Neuroprotective effects of brimonidine treatment in a rodent model of ischemic optic neuropathy, Danylkova NO; Alcala SR; Pomeranz HD et al., Experimental Eye Research, 2007; 84: 293-301

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Brimonidine was shown to be a powerful neuroprotective compound in several animal models of neural tissue insult. The effect observed, in all of the models, was protection from secondary degeneration imposed by the primary insult, regardless of its nature. In all these cases, brominidine was given as a therapeutic modality following the insult, to prevent degeneration of neurons that were spared in the primary insult, or to delay degeneration of severed axons. In models in which the therapeutic window is extremely narrow, however, the possibility that a neuroprotective intervention given after the insult could be of any benefit has been intensively studied. In the present study, Danylkova et al. (272) studied the potential of brimonidine as a neuroprotective agent in an animal model of ischemic optic neuropathy (ION), under the assumption that though it might not be effective in rescuing neurons within the injured eye, it may be useful as prophylactic protection for the other eye, which is often at risk of a delayed ION episode. The results of this study are promising and teach us that brimonidine can induce prophylactic neuroprotection, enabling the tissue at risk to be better 'prepared' to cope with the insult. It should be noted that based on the current understanding as to how brimonidine (an β2-adrenoreceptor agonist) acts as a neuroprotectant, its prophylactic effect could be manifest at the level of the eye, the optic nerve, or systemically. These findings do not imply that all neuroprotective therapies will work when prophylactically administered, but show that in the case of brimonidine, this approach can be effective.

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