Thanks. It looks like the protocol, not results, though.I found a manuscript. Not published per say.
Thanks. It looks like the protocol, not results, though.I found a manuscript. Not published per say.
In a recent study published in the journal Nutrients, Australian researchers reviewed the effects of coenzyme Q10 (CoQ10) supplementation on cognition. Approximately 22% of the world’s population is estimated to be 60 years or older by 2050. Accompanying this change will be an increase in people with cognitive decline and the prevalence of neurodegenerative diseases. The causes of neurodegenerative diseases and cognitive decline are multifactorial, but the major contributors are oxidative stress, inflammation, poor cardiovascular health, decreased cerebral blood flow, and mitochondrial dysfunction. These multiple processes in the body and brain require various targeted therapeutic approaches. Various approaches to addressing age-related cognitive decline have been employed, including dietary modifications, physical activity, medications, and nutritional supplements. CoQ10 is an antioxidant and metabolic stimulant that positively influences biological mechanisms relevant to cognition, with mixed effects on cognitive test performance in trials. In the present study, researchers reviewed the effects of CoQ10 supplementation on cognition.
![]()
Experts review the evidence on coenzyme Q10 and cognitive decline
Researchers reviewed evidence on coenzyme Q10 (CoQ10) and cognition, finding strong biological support and positive results in animal models but mixed outcomes in human trials. Larger, high-quality studies are needed to clarify whether CoQ10 can protect against cognitive decline and...www.news-medical.net
You asked me this question over 5 years ago and I wrote that I didn't know, but I put my glasses on this time and here is the result:What was the unit of measure @Mij?
Abstract
Ageing is associated with attenuated exercise responses in skeletal muscle, which may be related to a failure of muscle redox signalling. The attenuation of redox responses to exercise in aged muscle has been linked to perturbations in redox homeostasis induced by age-related increases in mitochondrial oxidative stress. Accordingly, we investigated the effects of supplementation with the mitochondria-targeted antioxidant MitoQ on mitochondrial bioenergetics and H2O2 emission as well as acute exercise-induced redox responses in skeletal muscle of older individuals. In a randomised, double-blind, placebo-controlled, parallel design, 10 males and 12 females aged 65–80 years were randomised to receive either MitoQ (20 mg/day) or a placebo for 12 weeks before completing a single bout of exercise. Vastus lateralis muscle biopsies were collected before supplementation and before, immediately post- and 4 h post-exercise. MitoQ supplementation reduced mitochondrial H2O2 emission capacity in skeletal muscle but did not impact mitochondrial respiration, H2O2 emission in the presence of ADP, or the sensitivity for ADP to stimulate respiration (apparent Km) and attenuate H2O2 emission (apparent IC50). Acute exercise-induced peroxiredoxin oxidation in skeletal muscle was not altered by MitoQ supplementation. Similarly, MitoQ had no effect on the phosphorylation of several redox-sensitive protein kinases (AMPK, p38 MAPK, and ERK1/2) or the upregulation of mitochondrial and antioxidant genes following exercise. Collectively, these findings indicate that MitoQ supplementation did not influence the basal myocellular redox state or redox responses to exercise in skeletal muscle of older individuals.