Functional rescue of experimental XXXX optic neuropathy with aB-crystallin.

@entity1018 @entity32 @entity6810 @entity63 @entity19 @entity1457 @entity989
PURPOSE: @entity6810 ( @entity6810 ) is an important cause of acute @entity1018 in adults, and there is no effective treatment. We studied early changes following experimental @entity6810 and tested the benefit of a potential treatment. MATERIALS AND METHODS: We induced experimental @entity6810 in adult @entity19 and tested the effects of short-term (daily for 3 days) and long-term (every other day for 3 weeks) aB-crystallin (aBC) treatment using histological and serial intracranial flash visual evoked potential recordings. RESULTS: One day after experimental @entity6810 , there was swelling at the optic nerve (ON) head and increased expression of aBC, a small @entity1457 protein important in @entity63 and @entity32 . This upregulation coincided with microglial and astrocytic activation. Our hypothesis was that aBC may be part of the endogenous protective mechanism against injury, thus we tested the effects of aBC on experimental @entity6810 . Daily intraveneous or intravitreal aBC injections did not improve visual evoked potential amplitude or latency at days 1-2. However, aBC treatment decreased swelling and dampened the microglial and astrocytic activation on day 3. Longer treatment with intravenous aBC led to acceleration of visual evoked potential latency over 3 weeks, without improving amplitude. This latency acceleration did not correlate with @entity989 cell survival but did correlate with complete rescue of the ON oligodendrocytes, which are important for myelination. CONCLUSIONS: We identified aBC as an early marker following experimental @entity6810 . Treatment with aBC enhanced this endogenous, post- @entity63 response by decreasing microglial activation and promoting ON oligodendrocyte survival.
