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. 2021 Jan 20;10(2):143.
doi: 10.3390/antiox10020143.

Ubiquinol Supplementation Improves Gender-Dependent Cerebral Vasoreactivity and Ameliorates Chronic Inflammation and Endothelial Dysfunction in Patients with Mild Cognitive Impairment

Affiliations

Ubiquinol Supplementation Improves Gender-Dependent Cerebral Vasoreactivity and Ameliorates Chronic Inflammation and Endothelial Dysfunction in Patients with Mild Cognitive Impairment

Sonia García-Carpintero et al. Antioxidants (Basel). .

Abstract

Ubiquinol can protect endothelial cells from multiple mechanisms that cause endothelial damage and vascular dysfunction, thus contributing to dementia. A total of 69 participants diagnosed with mild cognitive impairment (MCI) received either 200 mg/day ubiquinol (Ub) or placebo for 1 year. Cognitive assessment of patients was performed at baseline and after 1 year of follow-up. Patients' cerebral vasoreactivity was examined using transcranial Doppler sonography, and levels of Ub and lipopolysaccharide (LPS) in plasma samples were quantified. Cell viability and necrotic cell death were determined using the microvascular endothelial cell line bEnd3. Coenzyme Q10 (CoQ) levels increased in patients supplemented for 1 year with ubiquinol versus baseline and the placebo group, although higher levels were observed in male patients. The higher cCoQ concentration in male patients improved cerebral vasoreactivity CRV and reduced inflammation, although the effect of Ub supplementation on neurological improvement was negligible in this study. Furthermore, plasma from Ub-supplemented patients improved the viability of endothelial cells, although only in T2DM and hypertensive patients. This suggests that ubiquinol supplementation could be recommended to reach a concentration of 5 μg/mL in plasma in MCI patients as a complement to conventional treatment.

Keywords: LPS; breath holding index; coenzyme Q10; endothelial necrosis; mild cognitive impairment.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Plasma levels of Coenzyme Q10. Plasma levels of CoQ was evaluated by HPLC from plasma obtained from 69 patients at starting point (T0) and after 1-year supplementation (T1) with ubiquinol. (A) CoQ concentration in plasma from all patients enrolled and (B,C) split by sex, female and male, respectively. Values are represented in violin plots where mean and all points are indicated. Supplementation was considered for CoQ concentrations >2.1 µg/mL. Statistically significant differences were tested by Student t test, where ** and *** indicate p < 0.01 and p < 0.001, respectively.
Figure 2
Figure 2
Evaluation of breath-holding index evaluation. Mild cognitive impairment (MCI) was evaluated in 69 patients at starting point (T0) and after 1-year supplementation (T1) with ubiquinol. (A) Total patients who participated in the study. (B) Female. (C) Male. Values are represented in violin plots where mean and all points are indicated. Statistically significant differences were tested by Student t test, where * p < 0.05.
Figure 3
Figure 3
Total lipopolysaccharide (LPS) in plasma. LPS level was quantified in 69 patients at starting point (T0) and after 1-year supplementation (T1) with ubiquinol. (A) Total patients who participated in the study. (B) Female. (C) Male. Values, expressed as UE/mL of plasma, are represented in violin plots where mean and all points are indicated. Statistically significant differences were tested by Student t test, where * p < 0.05.
Figure 4
Figure 4
Correlation between Coenzyme Q10 concentration in plasma and necrotic cell death. Increment in CoQ concentration and in necrosis in T1-T0 are represented in X and Y axes, respectively. (A) Patients are stratified for Ub intake. (B) patients are stratified for Placebo intake. (C) Patients are stratified for type 2 diabetes mellitus. (D) Patients are stratified for hyperthension. Changes in variables were calculated as 1-year follow-up values minus baseline values.

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