Effectiveness of coenzyme Q10 on learning and memory and synaptic plasticity impairment in an aged Aβ-induced rat model of Alzheimer's disease: a behavioral, biochemical, and electrophysiological study
- PMID: 36811650
- DOI: 10.1007/s00213-023-06338-2
Effectiveness of coenzyme Q10 on learning and memory and synaptic plasticity impairment in an aged Aβ-induced rat model of Alzheimer's disease: a behavioral, biochemical, and electrophysiological study
Abstract
Rationale: Aging is the major risk factor for Alzheimer's disease (AD), and cognitive and memory impairments are common among the elderly. Interestingly, coenzyme Q10 (Q10) levels decline in the brain of aging animals. Q10 is a substantial antioxidant substance, which has an important role in the mitochondria.
Objective: We assessed the possible effects of Q10 on learning and memory and synaptic plasticity in aged β-amyloid (Aβ)-induced AD rats.
Methods: In this study, 40 Wistar rats (24-36 months old; 360-450 g) were randomly assigned to four groups (n = 10 rats/group)-group I: control, group II: Aβ, group III: Q10; 50 mg/kg, and group IV: Q10+Aβ. Q10 was administered orally by gavage daily for 4 weeks before the Aβ injection. The cognitive function and learning and memory of the rats were measured by the novel object recognition (NOR), Morris water maze (MWM), and passive avoidance learning (PAL) tests. Finally, malondialdehyde (MDA), total antioxidant capacity (TAC), total thiol group (TTG), and total oxidant status (TOS) were measured.
Results: Q10 improved the Aβ-related decrease in the discrimination index in the NOR test, spatial learning and memory in the MWM test, passive avoidance learning and memory in the PAL test, and long-term potentiation (LTP) impairment in the hippocampal PP-DG pathway in aged rats. In addition, Aβ injection significantly increased serum MDA and TOS levels. Q10, however, significantly reversed these parameters and also increased TAC and TTG levels in the Aβ+Q10 group.
Conclusions: Our experimental findings suggest that Q10 supplementation can suppress the progression of neurodegeneration that otherwise impairs learning and memory and reduces synaptic plasticity in our experimental animals. Therefore, similar supplemental Q10 treatment given to humans with AD could possibly provide them a better quality of life.
Keywords: Aging; Alzheimer’s disease; Amyloid-beta; Coenzyme Q10; Dentate gyrus; Hippocampus; Synaptic plasticity.
© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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