Investigation of protective effects of coenzyme Q10 on impaired synaptic plasticity in a male rat model of Alzheimer’s disease

Komaki, Hamidreza; Faraji, Nafiseh; Komaki‬, Alireza; Shahidi, Siamak; Etaee, Farshid; Raoufi, Safoura; Mirzaei, Fatemeh

doi:10.1016/j.brainresbull.2019.01.025

Cited by 63 publications

(36 citation statements)

References 75 publications

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“…Q10 is an important electron transporter of mitochondrial oxidative phosphorylation. In addition, Q10 has a protective effect on synaptic plasticity (24) and mitochondrial alterations (25). Q10 treatment for four weeks reversed the levels of retinal ATP contents, Mt CPX4-2, synaptic plasticity, PGC-1α, and TFAM to maintain retinal function.…”

Section: Discussionmentioning

confidence: 98%

Maternal high-fructose diet induced early-onset retinopathy via the suppression of synaptic plasticity mediated by mitochondrial dysfunction

Huang

Chen

et al. 2021

American Journal of Physiology-Endocrinology and Metabolism

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Retinopathy is a leading cause of blindness, and there is currently no cure. Earlier identification of the progression of retinopathy could provide a better chance for intervention. Diet has profound effects on retinal function. A maternal high fructose diet (HFD) triggers diseases in multiple organs. However, whether maternal HFD impairs retinal function in adult offspring is currently unknown. By using the rodent model of maternal HFD during pregnancy and lactation, our data indicated a reduced b-wave of electroretinography (ERG) in HFD female offspring at 3 months of age compared with age-matched offspring of dams fed regular chow (ND). Immunofluorescence and Western blot analyses indicated that the distributions and expressions of synaptophysin, postsynaptic density protein 95 (PSD95), and phospho(p)-Ca2+/calmodulin-stimulated protein kinase IIa (CaMKIIa) were significantly suppressed in the HFD group. Furthermore, the ATP content and the mitochondrial respiratory protein, Mt CPX 4-2, were decreased. Moreover, the expressions of peroxisome proliferator-activated receptor g coactivator 1-α (PGC-1α) and mitochondrial transcription factor A (TFAM) in the retina of the HFD group were downregulated. Treatment with coenzyme Q10 (Q10), a key mediator of the electron transport chain, effectively reversed these abovementioned dysfunctions. Together, these results suggested that maternal HFD impaired retinal function in adult female offspring. The mechanism underlying early-onset retinopathy may involve the reduction in the capacity of mitochondrial energy production and the suppression of synaptic plasticity. Most importantly, mitochondria could be a feasible target to reprogram maternal HFD-damaged retinal function.

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Section: Discussionmentioning

confidence: 98%

Maternal high-fructose diet induced early-onset retinopathy via the suppression of synaptic plasticity mediated by mitochondrial dysfunction

Huang

Chen

et al. 2021

American Journal of Physiology-Endocrinology and Metabolism

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“…They demonstrated that CoQ 10 supplementation increases long-term potentiation in both intact and β-amyloid-injected rats. Furthermore, CoQ 10 reversed the increases in serum MDA levels and total oxidative stress, indicating that CoQ 10 treatment changed the oxidant/antioxidant balance in favour of antioxidants [ 101 ].…”

Section: Coq 10 and Neurodegenerative Diseases mentioning

confidence: 99%

Coenzyme Q10 Supplementation for the Reduction of Oxidative Stress: Clinical Implications in the Treatment of Chronic Diseases

Gutiérrez-Mariscal

Larriva

Pérez

et al. 2020

IJMS

103

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Apart from its main function in the mitochondria as a key element in electron transport, Coenzyme Q10 (CoQ10) has been described as having multiple functions, such as oxidant action in the generation of signals and the control of membrane structure and phospholipid and cellular redox status. Among these, the most relevant and most frequently studied function is the potent antioxidant capability of its coexistent redox forms. Different clinical trials have investigated the effect of CoQ10 supplementation and its ability to reduce oxidative stress. In this review, we focused on recent advances in CoQ10 supplementation, its role as an antioxidant, and the clinical implications that this entails in the treatment of chronic diseases, in particular cardiovascular diseases, kidney disease, chronic obstructive pulmonary disease, non-alcoholic fatty liver disease, and neurodegenerative diseases. As an antioxidant, CoQ10 has proved to be of potential use as a treatment in diseases in which oxidative stress is a hallmark, and beneficial effects of CoQ10 have been reported in the treatment of chronic diseases. However, it is crucial to reach a consensus on the optimal dose and the use of different formulations, which vary from ubiquinol or ubiquinone Ubisol-Q10 or Qter®, to new analogues such as MitoQ, before we can draw a clear conclusion about its clinical use. In addition, a major effort must be made to demonstrate its beneficial effects in clinical trials, with a view to making the implementation of CoQ10 possible in clinical practice.

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“…Some investigations have remarked that oxidative stress causes neural injury in brain regions associated with the etiology of memory damage [65][66][67]. Furthermore, oxidative stress could influence synaptic plasticity and can lead to diminished LTP induction [40]. In contrast, some of the previous studies have shown that antioxidants improve the induction of hippocampal LTP [68].…”

Section: Discussionmentioning

confidence: 99%

“…Long-term potentiation (LTP) is a kind of synaptic plasticity, which is established as a long-lasting augmentation of synaptic communications [40]. This phenomenon in the hippocampus and elsewhere is a probable synaptic substrate of the long-term learning and memory modifications [41].…”

Section: Introductionmentioning

confidence: 99%

Effects of Hypericum scabrum extract on dentate gyrus synaptic plasticity in high fat diet-fed rats

et al. 2020

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High-fat diet (HFD) can induce deficits in neural function, oxidative stress, and decrease hippocampal neurogenesis. Hypericum (H.) scabrum extract (Ext) contains compounds that could treat neurological disorders. This study aimed to examine the neuroprotective impacts of the H. scabrum Ext on hippocampal synaptic plasticity in rats that were fed HFD. Fifty-four male Wistar rats (220 ± 10 g) were randomly arranged in six groups: (1) HFD group; (2) HFD + Ext300 group; (3) HFD + Ext100 group; (4) Control group; (5) Ext 300 mg/kg group; (6) Ext 100 mg/kg group. These protocols were administrated for 3 months. After this stage, a stimulating electrode was implanted in the perforant pathway (PP), and a bipolar recording electrode was embedded into the dentate gyrus (DG). Long-term potentiation (LTP) was provoked by high-frequency stimulation (HFS) of the PP. Field excitatory postsynaptic potentials (EPSP) and population spikes (PS) were recorded at 5, 30, and 60 min after HFS. The HFD group exhibited a large and significant decrease in their PS amplitude and EPSP slope as compared to the control and extract groups. In reverse, H. scabrum administration in the HFD + Ext rats reversed the effect of HFD on the PS amplitude and EPSP slope. The results of the study support that H. scabrum Ext can inhibit diminished synaptic plasticity caused by the HFD. These effects are probably due to the extreme antioxidant impacts of the Ext and its capability to scavenge free radicals.

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Investigation of protective effects of coenzyme Q10 on impaired synaptic plasticity in a male rat model of Alzheimer’s disease

Cited by 63 publications

References 75 publications

Maternal high-fructose diet induced early-onset retinopathy via the suppression of synaptic plasticity mediated by mitochondrial dysfunction

Maternal high-fructose diet induced early-onset retinopathy via the suppression of synaptic plasticity mediated by mitochondrial dysfunction

Coenzyme Q10 Supplementation for the Reduction of Oxidative Stress: Clinical Implications in the Treatment of Chronic Diseases

Effects of Hypericum scabrum extract on dentate gyrus synaptic plasticity in high fat diet-fed rats

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