RESUMEN
Oxidative stress plays a key role in contributing to ß-amyloid (Aß) deposition in Alzheimer's disease (AD). Coenzyme Q10 (Q10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals. In this study, we investigated the neuroprotective effects of Q10 on Aß-induced impairment in hippocampal long-term potentiation (LTP), a widely researched model of synaptic plasticity, which occurs during learning and memory, in a rat model of AD. In this study, 50 adult male Wistar rats were assigned to five groups: control group (saline); sham group; intraventricular PBS injection, Aß group; intraventricular Aß injection, Q10 group; and Q10 via oral gavage and Q10 + Aß group. Q10 was administered via oral gavage, once a day, for 3 weeks before and 3 weeks after the Aß injection. After the treatment period, in vivo electrophysiological recordings were performed to quantify the excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the hippocampal dentate gyrus. LTP was created by a high-frequency stimulation of the perforant pathway. Following LTP induction, the EPSP slope and PS amplitude were significantly diminished in Aß-injected rats, compared with sham and control rats. Q10 treatment of Aß-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Aß on LTP. Aß significantly increased serum malondialdehyde levels and total oxidant levels, whereas Q10 supplementation significantly reversed these parameters and increased total antioxidant capacity levels. The present findings suggested that Q10 treatment offers neuroprotection against the detrimental effects of Aß on hippocampal synaptic plasticity via its antioxidant activity.