Using coenzyme Q10 in clinical practice By Emily A. Brandmeyer, BSN, RN; Qiuhua Shen, PhD, APRN, RN; Amanda R. Thimmesch, BA; and Janet D. Pierce, PhD, APRN, CCRN, FAAN
COENZYME Q10 (CoQ10), a lipid-soluble, vitamin-like substance present in nearly all human tissues, is essential for the basic functioning of cells. Mainly produced in the mitochondria, it’s required for the production of adenosine triphosphate (ATP), which stores energy used to support cell growth and maintenance.1 CoQ10 is also an antioxidant that protects the body from damage caused by free radicals, which are highly reactive chemicals that can harm cells.2 As people age, their CoQ10 production decreases.1 Rich sources of dietary CoQ10 include meat, poultry, and fish. It can also be found in soybean and canola oil, nuts, eggs, and dairy products. However, a person deficient in CoQ10 would have to consume an enormous amount of these foods to supplement CoQ10 needs adequately.3 In patients with cardiovascular disease, diabetes, neurodegenerative disorders, and cancer, CoQ10 levels are insufficient to prevent free radical damage to protein, DNA, and lipids in the cells.4 Certain prescripwww.Nursing2014.com
tion drugs such as statins may lower CoQ10 levels. This article will review the cellular function of CoQ10 and how it’s used in clinical practice. Mitochondrial function To understand the effects of CoQ10, it’s important to review the anatomy and physiology of the mitochondrion, where CoQ10 is synthesized and used by cells. Mitochondria are known as “cellular power plants” because they generate most of the cell’s ATP. (See Inside the cellular power plant.) CoQ10 is found in the mitochondria in two forms: fully oxidized ubiquinone and reduced ubiquinol. Ubiquinone is converted to ubiquinol in a reduction reaction, during which the molecule gains two electrons. In order for the body to use CoQ10, it must undergo this reaction. Efficient reduction of CoQ10 to ubiquinol occurs rapidly after CoQ10 appears in the blood, carried by lipoproteins. As humans age, CoQ10 production decreases, and the ability to reduce March l Nursing2014 l 63
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
ubiquinone to ubiquinol in the mitochondria is impaired.5 Found in the inner membrane of the mitochondria, CoQ10 is involved in essential cellular processes of energy production. It acts as both an electron carrier and proton translocator during cellular respiration and ATP production.6 CoQ10 functions as an electron carrier from each enzyme complex down the electron transport chain (ETC). This action is crucial to ATP production.1 In its reduced form (ubiquinol), CoQ10 acts as a lipophilic antioxi-
dant in both the mitochondria and lipid membranes. As an antioxidant, CoQ10 is capable of recycling and regenerating other antioxidants, such as tocopherol and alpha-ascorbate. In contrast to other antioxidants, CoQ10 inhibits both the initiation and propagation of lipid and protein oxidation. This is very important to prevent oxidative damage caused by free radicals.7 Implications for practice The reduced form of CoQ10 (ubiquinol) is available as a dietary
supplement and has been used as a supplemental treatment for multiple diseases. Research has found that CoQ10 is an effective antioxidant that reduces damage to cellular mechanisms and can be useful in the treatment of the following conditions. Cardiovascular disorders Heart failure (HF) is a major healthcare issue in the United States, with over 5 million people diagnosed and 300,000 deaths from HF each year.8 The leading causes of HF are coronary
I LLUSTRATION BY THE KIDDRC I MAGING C ORE
Inside the cellular power plant
The mitochondria transform organic compounds into energy that’s easily accessible to the cell. They contain the enzymes needed for converting energy from food into cellular energy. Mitochondria are composed of two membranes: an outer membrane that encloses the periphery of the mitochondrion and an inner membrane that forms cristae, which expand the surface area of the inner membrane. Many chemical reactions that take place in the mitochondria occur in the inner membrane, which contains the ETC complexes I–V needed for the synthesis of ATP. These complexes help move electrons down the ETC. In between complexes I and II, two electrons are removed from the nicotinamide adenine dinucleotide structure and transferred to CoQ10, which become ubiquinol (reduced form). Ubiquinol is a lipid-soluble carrier for these electrons that facilitates the production of ATP.16
64 l Nursing2014 l March
www.Nursing2014.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
artery disease, hypertension, and diabetes. Depletion of energy in the myocardium is a dominant feature of HF. Reduced amounts of CoQ10 in myocardial tissues have been identified in patients with HF. Some clinicians use CoQ10 as a supplement to an HF medication regimen because it can help stabilize myocardial metabolism and maintain mitochondrial function.9 CoQ10 levels in the myocardial tissue are directly correlated to the severity of HF. Current studies have focused on CoQ10 treatment in HF to improve ejection fraction. Some studies have shown that oral CoQ10 might be helpful in improving functional capacity, endothelial function, and left ventricular contractility in patients with HF when taken in combination with other HF medications and treatment.9,10 A recent study showed that exercise, along with CoQ10 supplementation, resulted in higher plasma CoQ10 levels and improved ejection fraction with fewer HF symptoms. It also found that CoQ10 supplementation over a 2-year period may reduce unplanned cardiovascular hospitalization due to worsening HF and mortality.11 Patients with high cholesterol levels who are taking statins usually have lower levels of CoQ10 in tissues because statins interfere with the synthesis pathway of CoQ10. There’s some evidence that CoQ10 supplementation decreases myopathy associated with statin treatment.10,12 Research has also shown that CoQ10 has cardiac protective effects for patients with acute myocardial infarction and those who’ve undergone heart surgery.13 However, further studies are still needed to help establish the future role of CoQ10 in patients with cardiovascular disease. Diabetes Patients with type 1 or type 2 diabetes mellitus are frequently adwww.Nursing2014.com
mitted to hospitals with complications such as coronary artery disease, cerebrovascular disease, diabetic ketoacidosis, hyperglycemic crises, and peripheral neuropathy, one of the most common complications. CoQ10 can reduce peripheral neuropathy through its action as an antioxidant.14 It can also improve glycemic control in patients when given a daily oral dose in addition to their prescribed antihyperglycemic medications.15 Research has shown a significant improvement in A1C and glycemic control with the use of CoQ10.10 Better glycemic management may lead to a lower risk of diabetic complications and hospitalization. Neurodegenerative disorders CoQ10 has been used to reduce the symptoms of Parkinson, Huntington, and Alzheimer diseases.16,17 These conditions are partially caused by impairment of the ETC in the mitochondria and increased generation of reactive oxygen species.18,19 In Parkinson disease, CoQ10 has been shown to protect the nigrostriatal dopaminergic system, which is the major dopamine pathway connecting the stiatum and substantia nigra and contributing to movement function.20 Researchers found that daily oral CoQ10 supplementation for 16 months resulted in reported higher energy levels and increased CoQ10 levels in tissues. Improvements were seen in activities of daily living in the CoQ10 group compared with the control group.20 Other research has shown that CoQ10 supplementation only slows the decline of the disease in patients with early Parkinson disease and doesn’t improve symptoms in those with midstage disease.10 Adverse reactions and contraindications CoQ10 is naturally produced in the body, and the safety of high
doses of orally ingested CoQ10 for long periods is well established.3 It has an acceptable safety profile as a dietary supplement with multiple daily doses. Only mild gastrointestinal symptoms have been reported in a small number of subjects; these weren’t dose- related and occurred in both CoQ10 and placebo groups. 21 However, CoQ10 may interact with some medications such as warfarin, so advise patients to consult their healthcare provider before taking CoQ10. Supplement wisely CoQ10 is a safe, accessible treatment that may help reduce the signs and symptoms of many chronic conditions at a reasonable cost. Educate patients regarding CoQ10, its benefits when used for different conditions, and possible minor adverse reactions based on their medical history. For example, patients with HF or diabetes could take oral CoQ10 as an antioxidant and a new source of energy for the mitochondria. Assist patients with accurately monitoring CoQ10 doses based on their report of condition and improvement, and schedule follow-up visits to measure improvements in their health status. ■ REFERENCES 1. Bentinger M, Tekle M, Dallner G. Coenzyme Q—biosynthesis and functions. Biochem Biophys Res Commun. 2010;396(1):74-79. 2. National Cancer Institute. Antioxidants and cancer prevention. 2013. http://www.cancer.gov/ cancertopics/factsheet/prevention/antioxidants. 3. Pravst I, Zmitek K, Zmitek J. Coenzyme Q10 contents in foods and fortification strategies. Crit Rev Food Sci Nutr. 2010;50(4):269-280. 4. Lobo V, Patil A, Phatak A, Chandra N. Free radicals, antioxidants and functional foods: impact on human health. Pharmacogn Rev. 2010;4(8):118-126. 5. Tekin ED, Erkoc S. Structural and electronic features of the ubiquinone and ubiquinol molecules: molecular dynamics and quantum chemical treatments. Molecular Simulation. 2010; 36(10):763-771. 6. Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Devel. 2013; 3(1):13-17.
March l Nursing2014 l 65
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
7. Lee BJ, Huang YC, Chen SJ, Lin PT. Coenzyme Q10 supplementation reduces oxidative stress and increases antioxidant enzyme activity in patients with coronary artery disease. Nutrition. 2012;28(3): 250-255.
14. Shi TJ, Zhang MD, Zeberg H, et al. Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db-/db- mouse, a type 2 diabetes model. Proc Natl Acad Sci U S A. 2013;110(2): 690-695.
8. Lloyd-Jones D, Adams RJ, Brown TM, et al. Executive summary: heart disease and stroke statistics—2010 update: a report from the American Heart Association. Circulation. 2010;121(7): 948-954.
15. Mezawa M, Takemoto M, Onishi S, et al. The reduced form of coenzyme Q10 improves glycemic control in patients with type 2 diabetes: an open label pilot study. Biofactors. 2012;38(6):416-421.
9. Fotino AD, Thompson-Paul AM, Bazzano LA. Effect of coenzyme Q10 supplementation on heart failure: a meta-analysis. Am J Clin Nutr. 2013;97(2): 268-275.
16. Liu J, Wang L, Zhan SY, Xia Y. Coenzyme Q10 for Parkinson’s disease. Cochrane Database Syst Rev. 2011;(12):CD008150.
10. Medline Plus. Coenzyme Q-10. 2011. http:// www.nlm.nih.gov/medlineplus/druginfo/natural/ 938.html. 11. Belardinelli R, Muçaj A, Lacalaprice F, et al. Coenzyme Q10 and exercise training in chronic heart failure. Eur Heart J. 2006;27(22): 2675-2681. 12. Parker BA, Gregory SM, Lorson L, Polk D, White CM, Thompson PD. A randomized trial of coenzyme Q10 in patients with statin myopathy: rationale and study design. J Clin Lipidol. 2013;7(3): 187-193. 13. Ivanov AV, Gorodetskaya EA, Kalenikova EI, Medvedev OS. Single intravenous injection of coenzyme Q10 protects the myocardium after irreversible ischemia. Bull Exp Biol Med. 2013;155(6): 771-774.
17. Dumont M, Kipiani K, Yu F, et al. Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer’s disease. J Alzheimers Dis. 2011;27(1):211-223. 18. Exner N, Lutz AK, Haass C, Winklhofer KF. Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences. EMBO J. 2012;31(14):3038-3062. 19. Aliev G, Priyadarshini M, Reddy VP, et al. Oxidative stress mediated mitochondrial and vascular lesions as markers in the pathogenesis of Alzheimer disease. Curr Med Chem. [E-pub Dec. 27, 2013.] 20. Santos CM. New agents promote neuroprotection in Parkinson’s disease models. CNS Neurol Disord Drug Targets. 2012;11(4):410-418.
21. Hosoe K, Kitano M, Kishida H, Kubo H, Fujii K, Kitahara M. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007;47 (1):19-28.
Emily A. Brandmeyer is a staff nurse at Via Christi Hospital in Wichita, Kan. Qiuhua Shen is an assistant professor; Amanda R. Thimmesch is a research associate; and Janet D. Pierce is a professor, all at the University of Kansas School of Nursing in Kansas City.
Acknowledgment: This research was sponsored by the TriService Nursing Research Program, Uniformed Services University of the Health Sciences (HU000111-1-TS09); however, the information or content and conclusions do not necessarily represent the official position or policy of, nor should any official endorsement be inferred by, the TriService Nursing Research Program, Uniformed Services University of the Health Sciences, the Department of Defense, or the U.S. Government.
The authors have disclosed that they have no financial relationships related to this article.
DOI-10.1097/01.NURSE.0000443317.81231.d3
Don’t forget Facebook… Check out Nursing2014 on Facebook! Search for “NsgJournal” and click “like” to subscribe. We post breaking nursing news and provide links to articles on our website. Stay ahead of the game and “like” us today!
66 l Nursing2014 l March
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Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
COENZYME Q10 (CoQ10), a lipid-soluble, vitamin-like substance present in nearly all human tissues, is essential for the basic functioning of cells. Mainly produced in the mitochondria, it’s required for the production of adenosine triphosphate (ATP), which stores energy used to support cell growth and maintenance.1 CoQ10 is also an antioxidant that protects the body from damage caused by free radicals, which are highly reactive chemicals that can harm cells.2 As people age, their CoQ10 production decreases.1 Rich sources of dietary CoQ10 include meat, poultry, and fish. It can also be found in soybean and canola oil, nuts, eggs, and dairy products. However, a person deficient in CoQ10 would have to consume an enormous amount of these foods to supplement CoQ10 needs adequately.3 In patients with cardiovascular disease, diabetes, neurodegenerative disorders, and cancer, CoQ10 levels are insufficient to prevent free radical damage to protein, DNA, and lipids in the cells.4 Certain prescripwww.Nursing2014.com
tion drugs such as statins may lower CoQ10 levels. This article will review the cellular function of CoQ10 and how it’s used in clinical practice. Mitochondrial function To understand the effects of CoQ10, it’s important to review the anatomy and physiology of the mitochondrion, where CoQ10 is synthesized and used by cells. Mitochondria are known as “cellular power plants” because they generate most of the cell’s ATP. (See Inside the cellular power plant.) CoQ10 is found in the mitochondria in two forms: fully oxidized ubiquinone and reduced ubiquinol. Ubiquinone is converted to ubiquinol in a reduction reaction, during which the molecule gains two electrons. In order for the body to use CoQ10, it must undergo this reaction. Efficient reduction of CoQ10 to ubiquinol occurs rapidly after CoQ10 appears in the blood, carried by lipoproteins. As humans age, CoQ10 production decreases, and the ability to reduce March l Nursing2014 l 63
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
ubiquinone to ubiquinol in the mitochondria is impaired.5 Found in the inner membrane of the mitochondria, CoQ10 is involved in essential cellular processes of energy production. It acts as both an electron carrier and proton translocator during cellular respiration and ATP production.6 CoQ10 functions as an electron carrier from each enzyme complex down the electron transport chain (ETC). This action is crucial to ATP production.1 In its reduced form (ubiquinol), CoQ10 acts as a lipophilic antioxi-
dant in both the mitochondria and lipid membranes. As an antioxidant, CoQ10 is capable of recycling and regenerating other antioxidants, such as tocopherol and alpha-ascorbate. In contrast to other antioxidants, CoQ10 inhibits both the initiation and propagation of lipid and protein oxidation. This is very important to prevent oxidative damage caused by free radicals.7 Implications for practice The reduced form of CoQ10 (ubiquinol) is available as a dietary
supplement and has been used as a supplemental treatment for multiple diseases. Research has found that CoQ10 is an effective antioxidant that reduces damage to cellular mechanisms and can be useful in the treatment of the following conditions. Cardiovascular disorders Heart failure (HF) is a major healthcare issue in the United States, with over 5 million people diagnosed and 300,000 deaths from HF each year.8 The leading causes of HF are coronary
I LLUSTRATION BY THE KIDDRC I MAGING C ORE
Inside the cellular power plant
The mitochondria transform organic compounds into energy that’s easily accessible to the cell. They contain the enzymes needed for converting energy from food into cellular energy. Mitochondria are composed of two membranes: an outer membrane that encloses the periphery of the mitochondrion and an inner membrane that forms cristae, which expand the surface area of the inner membrane. Many chemical reactions that take place in the mitochondria occur in the inner membrane, which contains the ETC complexes I–V needed for the synthesis of ATP. These complexes help move electrons down the ETC. In between complexes I and II, two electrons are removed from the nicotinamide adenine dinucleotide structure and transferred to CoQ10, which become ubiquinol (reduced form). Ubiquinol is a lipid-soluble carrier for these electrons that facilitates the production of ATP.16
64 l Nursing2014 l March
www.Nursing2014.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
artery disease, hypertension, and diabetes. Depletion of energy in the myocardium is a dominant feature of HF. Reduced amounts of CoQ10 in myocardial tissues have been identified in patients with HF. Some clinicians use CoQ10 as a supplement to an HF medication regimen because it can help stabilize myocardial metabolism and maintain mitochondrial function.9 CoQ10 levels in the myocardial tissue are directly correlated to the severity of HF. Current studies have focused on CoQ10 treatment in HF to improve ejection fraction. Some studies have shown that oral CoQ10 might be helpful in improving functional capacity, endothelial function, and left ventricular contractility in patients with HF when taken in combination with other HF medications and treatment.9,10 A recent study showed that exercise, along with CoQ10 supplementation, resulted in higher plasma CoQ10 levels and improved ejection fraction with fewer HF symptoms. It also found that CoQ10 supplementation over a 2-year period may reduce unplanned cardiovascular hospitalization due to worsening HF and mortality.11 Patients with high cholesterol levels who are taking statins usually have lower levels of CoQ10 in tissues because statins interfere with the synthesis pathway of CoQ10. There’s some evidence that CoQ10 supplementation decreases myopathy associated with statin treatment.10,12 Research has also shown that CoQ10 has cardiac protective effects for patients with acute myocardial infarction and those who’ve undergone heart surgery.13 However, further studies are still needed to help establish the future role of CoQ10 in patients with cardiovascular disease. Diabetes Patients with type 1 or type 2 diabetes mellitus are frequently adwww.Nursing2014.com
mitted to hospitals with complications such as coronary artery disease, cerebrovascular disease, diabetic ketoacidosis, hyperglycemic crises, and peripheral neuropathy, one of the most common complications. CoQ10 can reduce peripheral neuropathy through its action as an antioxidant.14 It can also improve glycemic control in patients when given a daily oral dose in addition to their prescribed antihyperglycemic medications.15 Research has shown a significant improvement in A1C and glycemic control with the use of CoQ10.10 Better glycemic management may lead to a lower risk of diabetic complications and hospitalization. Neurodegenerative disorders CoQ10 has been used to reduce the symptoms of Parkinson, Huntington, and Alzheimer diseases.16,17 These conditions are partially caused by impairment of the ETC in the mitochondria and increased generation of reactive oxygen species.18,19 In Parkinson disease, CoQ10 has been shown to protect the nigrostriatal dopaminergic system, which is the major dopamine pathway connecting the stiatum and substantia nigra and contributing to movement function.20 Researchers found that daily oral CoQ10 supplementation for 16 months resulted in reported higher energy levels and increased CoQ10 levels in tissues. Improvements were seen in activities of daily living in the CoQ10 group compared with the control group.20 Other research has shown that CoQ10 supplementation only slows the decline of the disease in patients with early Parkinson disease and doesn’t improve symptoms in those with midstage disease.10 Adverse reactions and contraindications CoQ10 is naturally produced in the body, and the safety of high
doses of orally ingested CoQ10 for long periods is well established.3 It has an acceptable safety profile as a dietary supplement with multiple daily doses. Only mild gastrointestinal symptoms have been reported in a small number of subjects; these weren’t dose- related and occurred in both CoQ10 and placebo groups. 21 However, CoQ10 may interact with some medications such as warfarin, so advise patients to consult their healthcare provider before taking CoQ10. Supplement wisely CoQ10 is a safe, accessible treatment that may help reduce the signs and symptoms of many chronic conditions at a reasonable cost. Educate patients regarding CoQ10, its benefits when used for different conditions, and possible minor adverse reactions based on their medical history. For example, patients with HF or diabetes could take oral CoQ10 as an antioxidant and a new source of energy for the mitochondria. Assist patients with accurately monitoring CoQ10 doses based on their report of condition and improvement, and schedule follow-up visits to measure improvements in their health status. ■ REFERENCES 1. Bentinger M, Tekle M, Dallner G. Coenzyme Q—biosynthesis and functions. Biochem Biophys Res Commun. 2010;396(1):74-79. 2. National Cancer Institute. Antioxidants and cancer prevention. 2013. http://www.cancer.gov/ cancertopics/factsheet/prevention/antioxidants. 3. Pravst I, Zmitek K, Zmitek J. Coenzyme Q10 contents in foods and fortification strategies. Crit Rev Food Sci Nutr. 2010;50(4):269-280. 4. Lobo V, Patil A, Phatak A, Chandra N. Free radicals, antioxidants and functional foods: impact on human health. Pharmacogn Rev. 2010;4(8):118-126. 5. Tekin ED, Erkoc S. Structural and electronic features of the ubiquinone and ubiquinol molecules: molecular dynamics and quantum chemical treatments. Molecular Simulation. 2010; 36(10):763-771. 6. Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Devel. 2013; 3(1):13-17.
March l Nursing2014 l 65
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
7. Lee BJ, Huang YC, Chen SJ, Lin PT. Coenzyme Q10 supplementation reduces oxidative stress and increases antioxidant enzyme activity in patients with coronary artery disease. Nutrition. 2012;28(3): 250-255.
14. Shi TJ, Zhang MD, Zeberg H, et al. Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db-/db- mouse, a type 2 diabetes model. Proc Natl Acad Sci U S A. 2013;110(2): 690-695.
8. Lloyd-Jones D, Adams RJ, Brown TM, et al. Executive summary: heart disease and stroke statistics—2010 update: a report from the American Heart Association. Circulation. 2010;121(7): 948-954.
15. Mezawa M, Takemoto M, Onishi S, et al. The reduced form of coenzyme Q10 improves glycemic control in patients with type 2 diabetes: an open label pilot study. Biofactors. 2012;38(6):416-421.
9. Fotino AD, Thompson-Paul AM, Bazzano LA. Effect of coenzyme Q10 supplementation on heart failure: a meta-analysis. Am J Clin Nutr. 2013;97(2): 268-275.
16. Liu J, Wang L, Zhan SY, Xia Y. Coenzyme Q10 for Parkinson’s disease. Cochrane Database Syst Rev. 2011;(12):CD008150.
10. Medline Plus. Coenzyme Q-10. 2011. http:// www.nlm.nih.gov/medlineplus/druginfo/natural/ 938.html. 11. Belardinelli R, Muçaj A, Lacalaprice F, et al. Coenzyme Q10 and exercise training in chronic heart failure. Eur Heart J. 2006;27(22): 2675-2681. 12. Parker BA, Gregory SM, Lorson L, Polk D, White CM, Thompson PD. A randomized trial of coenzyme Q10 in patients with statin myopathy: rationale and study design. J Clin Lipidol. 2013;7(3): 187-193. 13. Ivanov AV, Gorodetskaya EA, Kalenikova EI, Medvedev OS. Single intravenous injection of coenzyme Q10 protects the myocardium after irreversible ischemia. Bull Exp Biol Med. 2013;155(6): 771-774.
17. Dumont M, Kipiani K, Yu F, et al. Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer’s disease. J Alzheimers Dis. 2011;27(1):211-223. 18. Exner N, Lutz AK, Haass C, Winklhofer KF. Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences. EMBO J. 2012;31(14):3038-3062. 19. Aliev G, Priyadarshini M, Reddy VP, et al. Oxidative stress mediated mitochondrial and vascular lesions as markers in the pathogenesis of Alzheimer disease. Curr Med Chem. [E-pub Dec. 27, 2013.] 20. Santos CM. New agents promote neuroprotection in Parkinson’s disease models. CNS Neurol Disord Drug Targets. 2012;11(4):410-418.
21. Hosoe K, Kitano M, Kishida H, Kubo H, Fujii K, Kitahara M. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007;47 (1):19-28.
Emily A. Brandmeyer is a staff nurse at Via Christi Hospital in Wichita, Kan. Qiuhua Shen is an assistant professor; Amanda R. Thimmesch is a research associate; and Janet D. Pierce is a professor, all at the University of Kansas School of Nursing in Kansas City.
Acknowledgment: This research was sponsored by the TriService Nursing Research Program, Uniformed Services University of the Health Sciences (HU000111-1-TS09); however, the information or content and conclusions do not necessarily represent the official position or policy of, nor should any official endorsement be inferred by, the TriService Nursing Research Program, Uniformed Services University of the Health Sciences, the Department of Defense, or the U.S. Government.
The authors have disclosed that they have no financial relationships related to this article.
DOI-10.1097/01.NURSE.0000443317.81231.d3
Don’t forget Facebook… Check out Nursing2014 on Facebook! Search for “NsgJournal” and click “like” to subscribe. We post breaking nursing news and provide links to articles on our website. Stay ahead of the game and “like” us today!
66 l Nursing2014 l March
www.Nursing2014.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
