Publications by authors named "Iain Hargreaves"
Article Synopsis
- * In the mitochondria, ubiquinone is converted to ubiquinol by Complexes I and II, while Complex III reverts ubiquinol back to ubiquinone, with additional enzymes aiding in this redox cycle.
- * The article discusses the clinical implications of deficiencies in this redox cycle and highlights the potential benefits of CoQ10 and selenium co-supplementation for health.
Article Synopsis
- Parkinson's disease (PD) is a common neurodegenerative disorder linked to environmental factors like exposure to the neurotoxin rotenone, which disrupts mitochondrial function and harms dopaminergic neurons.
- The study aimed to explore how rotenone affects mitochondrial dysfunction and oxidative stress in SH-SY5Y neuronal cells and to see if Coenzyme Q (CoQ) could help reduce this stress.
- Findings showed that rotenone significantly inhibited mitochondrial enzyme activity and increased oxidative stress, but CoQ supplementation effectively lowered reactive oxygen species production and alleviated some of the neuronal damage.
Efficacy and Safety of Coenzyme Q10 Supplementation in Neonates, Infants and Children: An Overview.
Antioxidants (Basel)
April 2024
Article Synopsis
- This article is the first to review the effectiveness and safety of coenzyme Q10 (CoQ10) supplementation specifically in younger populations, including neonates, infants, and children.
- It focuses on cases where CoQ10 supplementation is used due to various medical disorders rather than for healthy individuals, as there is no established need for it in otherwise healthy younger subjects.
- The review covers a range of clinical conditions, such as CoQ10 deficiency, muscular dystrophy, migraines, and other specific health issues in children.
Article Synopsis
- - There are about 90 different autoimmune disorders that impact various tissues in the body and can be challenging to treat effectively.
- - These disorders typically involve issues like mitochondrial dysfunction, oxidative stress, and inflammation, which has led researchers to consider coenzyme Q10 (CoQ10) as a potential treatment option due to its roles in mitochondrial health and as an antioxidant.
- - The article reviews how both a lack of CoQ10 and its supplementation may positively influence the management of various autoimmune disorders.
Article Synopsis
- * The most common side effect is statin-induced myopathy, which involves muscle pain and weakness and is linked to high levels of a muscle enzyme called creatine kinase.
- * Researchers believe that the cause of this myopathy may involve problems with mitochondria, possibly due to reduced coenzyme Q production, disrupted calcium signaling, and changes in reactive oxygen species levels.
Article Synopsis
- Post-viral fatigue syndrome (PVFS) involves various complex disorders characterized by severe fatigue, muscle and joint pain, cognitive issues, poor sleep quality, autonomic dysfunction, and neuropsychiatric symptoms, including ME/CFS and long COVID.
- There are currently no established clinical guidelines or FDA-approved treatments for PVFS, leading to a pressing need for new therapeutic approaches.
- Recent research highlights the potential role of mitochondrial dysfunction in PVFS conditions, and this article specifically reviews how coenzyme Q10 supplementation could help alleviate chronic fatigue and pain symptoms in these disorders.
Article Synopsis
- Coenzyme Q10 (CoQ10) is crucial for cellular functions, acting as an antioxidant and supporting processes like fatty acid metabolism and gene expression.
- Deficiencies in CoQ10 can lead to various health disorders, classified into primary (from genetic mutations) and secondary types.
- The article reviews clinical studies on CoQ10 supplementation, its therapeutic potential, ongoing debates about its effectiveness, and highlights unresolved issues needing further investigation.
Originally identified as a key component of the mitochondrial respiratory chain, Coenzyme Q (CoQ or CoQ for human tissues) has recently been revealed to be essential for many different redox processes, not only in the mitochondria, but elsewhere within other cellular membrane types. Cells rely on endogenous CoQ biosynthesis, and defects in this still-not-completely understood pathway result in primary CoQ deficiencies, a group of conditions biochemically characterised by decreased tissue CoQ levels, which in turn are linked to functional defects. Secondary CoQ deficiencies may result from a wide variety of cellular dysfunctions not directly linked to primary synthesis.
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- Mitochondria are essential for immune responses, and their function can be affected by viruses, which may influence the outcomes of COVID-19 and long COVID in patients.
- Patients with existing mitochondrial respiratory chain (MRC) disorders could be at a greater risk for severe outcomes from COVID-19 due to MRC dysfunction.
- A combination of diagnostic approaches, including metabolic profiling and measuring specific biomarkers like lactate and FGF-21, can help identify mitochondrial dysfunction in patients affected by COVID-19.
Article Synopsis
- Mitochondrial dysfunction and oxidative stress may contribute to various endocrine disorders, highlighting the potential benefits of coenzyme Q10 (CoQ10) due to its protective roles in mitochondria and as an antioxidant.
- The article reviews the impact of CoQ10 deficiency and supplementation specifically in relation to thyroid issues, diabetes, male infertility, and polycystic ovary syndrome.
- Focus areas include conditions like hyperthyroidism and type II diabetes, suggesting CoQ10 could play a significant role in managing these health issues.
Article Synopsis
- * Key questions explored include ways to improve CoQ10's bioavailability, potential intravenous administration, its ability to cross the blood-brain barrier, and how it is transported within cells.
- * The article emphasizes the need for further research to understand why some trials have failed and to identify the best tissues for assessing CoQ10 levels clinically.
Depletion and Supplementation of Coenzyme Q10 in Secondary Deficiency Disorders.
Front Biosci (Landmark Ed)
December 2022
Coenzyme Q10 (CoQ10) deficiency is broadly divided into two types, primary and secondary. Primary CoQ10 deficiencies are relatively rare disorders resulting from mutations in genes directly involved in the CoQ10 biosynthetic pathway, and are not a subject of this article. Secondary CoQ10 disorders are relatively common, and may occur for a variety of reasons; these include mutations in genes not directly related to the synthetic pathway, oxidative stress induced reduction of CoQ10, and the effects of pharmacological agents such as statins.
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- The article explores the role of coenzyme Q10 (CoQ10) in treating various less common age-related disorders, many of which currently lack effective treatments.
- It highlights how mitochondrial dysfunction, oxidative stress, and inflammation are involved in these diseases, suggesting that CoQ10 could be beneficial due to its functions as a mitochondrial supporter, antioxidant, and anti-inflammatory agent.
- Disorders discussed include multi system atrophy, progressive supranuclear palsy, sporadic adult onset ataxia, pulmonary fibrosis, and several others linked to aging and mitochondrial issues.
Odd- and even-numbered medium-chained fatty acids protect against glutathione depletion in very long-chain acyl-CoA dehydrogenase deficiency.
Biochim Biophys Acta Mol Cell Biol Lipids
February 2023
Article Synopsis
- Recent trials suggest that triheptanoin may help with severe symptoms of long-chain fatty acid oxidation disorders, notably in patients with VLCAD deficiency, though milder symptoms remain difficult to treat.
- This study explores how medium-chain fatty acids, like octanoate and heptanoate, can protect VLCAD-deficient cells from oxidative stress-induced depletion of the antioxidant glutathione (GSH).
- Results indicate that increasing medium-chain fatty acid concentrations can help retain GSH during metabolic stress, while lower glutamine levels lead to GSH depletion, which can be reversed by these fatty acids in a dose-dependent manner.
Article Synopsis
- - Mitochondrial dysfunction is linked to several neurodegenerative diseases, such as Parkinson's and Alzheimer's, due to its reduced ability to produce ATP, the energy currency of cells.
- - The article discusses how a deficiency in certain nutrients can further impair mitochondrial function, potentially worsening these conditions.
- - It suggests that supplements like CoQ10, B-vitamins/NADH, L-carnitine, vitamin D, and alpha-lipoic acid may help improve mitochondrial health and aid in treating these neurodegenerative diseases.
The aim of this study was to investigate coenzyme Q10 (CoQ) biosynthesis pathway defects in inherited retinal dystrophy. Individuals affected by inherited retinal dystrophy (IRD) underwent exome or genome sequencing for molecular diagnosis of their condition. Following negative IRD gene panel analysis, patients carrying biallelic variants in CoQ biosynthesis pathway genes were identified.
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- * Common issues leading to this dysfunction seem to involve oxidative stress and impaired mitophagy, contributing to neurodegeneration that is difficult to treat.
- * The review suggests exploring new therapies that address both mitochondrial and lysosomal impairment, aiming to improve treatment for long-term complications in patients with LSDs.
Mitochondrial dysfunction is a key pathological driver of early stage Parkinson's.
Acta Neuropathol Commun
September 2022
Article Synopsis
- The study investigates the molecular causes of early sporadic Parkinson's disease (PD) by analyzing brain tissues from affected individuals at Braak stages 3 and 4, focusing on different severity levels of alpha-synuclein inclusions and neuronal loss.
- Using advanced techniques, researchers compared protein expression across multiple brain regions and found that early changes occur in energy metabolism and mitochondrial function before significant cell damage happens.
- Key findings suggest that mitochondrial dysfunction may play a crucial role in the early development of PD, indicating that targeting these metabolic changes could be essential for understanding and potentially treating the disease.
Article Synopsis
- * Some people may experience severe COVID-19 symptoms or long-term effects (long COVID) due to low levels of CoQ10 in their cells.
- * Researchers developed a method using HPLC and UV detection to measure CoQ10 levels in patient tissues, which could help identify individuals at risk for severe COVID-19 outcomes related to CoQ10 deficiency.
Article Synopsis
- * Initial tests involve analyzing metabolites in blood and urine, including measuring lactate, pyruvate, amino acids, and using organic acids, with new approaches like FGF-21 being explored.
- * Currently, the most reliable method for diagnosing MRC dysfunction is spectrophotometric analysis of enzyme activities from muscle or affected tissues, due to a lack of good biomarkers.
Article Synopsis
- Lyme disease is caused by a bacterial infection from an infected tick bite, and initial treatment involves antibiotics; delayed treatment can lead to fatigue and issues with the nervous, cardiovascular, and joint systems.
- Damage in these areas is primarily due to the body's extreme inflammatory response, which creates a vicious cycle of mitochondrial dysfunction and oxidative stress.
- The article explores the potential use of coenzyme Q10 (CoQ10) as a supplement to help improve mitochondrial function and reduce inflammation and oxidative stress in Lyme disease patients.
Article Synopsis
- * Coenzyme Q10, a vitamin-like substance, may offer therapeutic benefits for these disorders by supporting mitochondrial function and acting as an antioxidant.
- * This review focuses on human studies rather than animal research, discussing the outcomes of clinical trials involving coenzyme Q10 supplementation for age-related neurological disorders.
Article Synopsis
- Neurodegenerative diseases often impair nervous system function due to mitochondrial dysfunction and oxidative stress, which are major contributors to neurodegeneration.
- The brain is particularly vulnerable to oxidative damage because of its high energy needs and weak antioxidant defenses, leading to further tissue damage and neuroinflammation when imbalances occur.
- Targeting mitochondrial dysfunction through pharmacological interventions, like enhancing mitochondrial biogenesis or activating antioxidant pathways, has emerged as a promising therapeutic strategy to mitigate neurodegeneration, with compounds like natural polyphenols and Nrf2 activators showing potential benefits.
Objective: This study investigated the effect of maternal obesity on aged-male offspring liver phenotype and hepatic expression of a programmed miRNA.
Methods: A mouse model (C57BL/6 J) of maternal diet-induced obesity was used to investigate fasting-serum metabolites, hepatic lipid content, steatosis, and relative mRNA levels (RT-PCR) and protein expression (Western blotting) of key components involved in hepatic and mitochondrial metabolism in 12-month-old offspring. We also measured hepatic lipid peroxidation, mitochondrial content, fibrosis stage, and apoptosis in the offspring.
Maternal obesity is a global problem that increases the risk of short- and long-term adverse outcomes for mother and child, many of which are linked to gestational diabetes mellitus. Effective treatments are essential to prevent the transmission of poor metabolic health from mother to child. Metformin is an effective glucose lowering drug commonly used to treat gestational diabetes mellitus; however, its wider effects on maternal and fetal health are poorly explored.
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