Brain-derived neurotrophic factor (
BDNF) could be considered a potential neuroprotective
therapy in
amyloid beta (Aβ)-associated
retinal and optic nerve degeneration. Hence, in this study we investigated the
neuroprotective effect of
BDNF against Aβ1-40-induced
retinal and
optic nerve injury. In this study, exposure to Aβ1-40 was associated with
retinal and
optic nerve injury. TUNEL staining showed significant reduction in the apoptotic cell count in the
BDNF-treated group compared with Aβ1-40 group. H&E-stained
retinal sections also showed a striking reduction in neuronal cells in the
ganglion cell layer (GCL) of retinas fourteen days after Aβ1-40 exposure. By contrast, number of
retinal cells was preserved in the retinas of
BDNF-treated animals. After Aβ1-40 exposure, visible axonal swelling was observed in optic nerve sections. However, the
BDNF-treated group showed fewer changes in optic nerve; axonal swelling was less frequent and less marked. In the present study, exposure to Aβ was associated with oxidative stress, whereas levels of
retinal glutathione (GSH),
superoxide dismutase (SOD) and
catalase were significantly increased in
BDNF-treated than in Aβ1-40-treated rats. Both visual object recognition tests using an open-field arena and a Morris water maze showed that
BDNF improved rats' ability to recognise visual cues (objects with different shapes) after Aβ1-40 exposure, thus demonstrating that the visual performance of rats was relatively preserved following
BDNF treatment. In conclusion, intravitreal treatment with
BDNF prevents Aβ1-40-induced
retinal cell apoptosis and axon loss in the optic nerve of rats by reducing
retinal oxidative stress and restoring
retinal BDNF levels.