4.4 Article

Effectiveness of coenzyme Q10 on learning and memory and synaptic plasticity impairment in an aged A beta-induced rat model of Alzheimer's disease: a behavioral, biochemical, and electrophysiological study

Journal

PSYCHOPHARMACOLOGY
Volume 240, Issue 4, Pages 951-967

Publisher

SPRINGER
DOI: 10.1007/s00213-023-06338-2

Keywords

Alzheimer's disease; Coenzyme Q10; Hippocampus; Synaptic plasticity; Dentate gyrus; Amyloid-beta; Aging

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This study found that coenzyme Q10 levels decline in aging animals, leading to the development of neurodegenerative diseases and impairments in memory and learning. However, oral supplementation of coenzyme Q10 can improve cognitive function, learning and memory, and enhance synaptic plasticity in aged animals. Therefore, providing coenzyme Q10 supplements to the elderly may improve their quality of life.
RationaleAging 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.ObjectiveWe assessed the possible effects of Q10 on learning and memory and synaptic plasticity in aged beta-amyloid (A beta)-induced AD rats.MethodsIn 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: A beta, group III: Q10; 50 mg/kg, and group IV: Q10+A beta. Q10 was administered orally by gavage daily for 4 weeks before the A beta 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.ResultsQ10 improved the A beta-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, A beta injection significantly increased serum MDA and TOS levels. Q10, however, significantly reversed these parameters and also increased TAC and TTG levels in the A beta+Q10 group.ConclusionsOur 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.

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