This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The purpose of this study is to assess the effects of CoQ on slowing the progressive impairment of Parkinson disease in early, otherwise untreated subjects. Parkinson disease (PD) is a progressive, neurodegenerative disease that affects over 1,000,000 Americans. It affects approximately one percent of persons over the age of 65. Coenzyme Q10 (CoQ) (2,3-dimethoxy-5-methylbenzoquinone), also known as ubiquinone, is a lipid-soluble benzoquinone derivative structurally similar to vitamin K. It is classified as a dietary supplement and is available commercially to the public over-the-counter (OTC). CoQ occurs naturally and is present in relatively high concentrations in the heart, liver, kidney and pancreas. Intracellular synthesis is the major source of CoQ, although some of it is acquired through the diet. Levels of CoQ from various tissues, including the brain, decline in humans with aging (Ernester and Dallner, 1995). The reasons for this decline and the contribution that the decline may have to diseases that occur more commonly in the elderly remain uncertain. Reduced levels of CoQ have been reported patients with heart failure, cardomyopathies, cancer, and some neurological diseases, including Parkinson disease (Ernster et al., 1995;Matsubara et al., 1991;Molina et al., 2002;Musumeci et al., 2001;Pepping 1999;Yamagami et al., 1981). An NIH-supported phase II trial (Shults et al., 2002) demonstrated that treatment of early Parkinson disease subjects with high dosages of CoQ was safe and well tolerated. There was a positive trend for treatment with CoQ to slow the progressive impairment. This phase III study is designed to confirm and extend the results of the phase II study.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000827-35
Application #
8166935
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2009-12-01
Project End
2010-06-30
Budget Start
2009-12-01
Budget End
2010-06-30
Support Year
35
Fiscal Year
2010
Total Cost
$4,142
Indirect Cost
Name
University of California San Diego
Department
Type
Schools of Medicine
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Grams, Morgan E; Sang, Yingying; Ballew, Shoshana H et al. (2018) Predicting timing of clinical outcomes in patients with chronic kidney disease and severely decreased glomerular filtration rate. Kidney Int 93:1442-1451
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Juraschek, Stephen P; Appel, Lawrence J; Miller 3rd, Edgar R (2017) Metoprolol Increases Uric Acid and Risk of Gout in African Americans With Chronic Kidney Disease Attributed to Hypertension. Am J Hypertens 30:871-875
Chen, Teresa K; Tin, Adrienne; Peralta, Carmen A et al. (2017) APOL1 Risk Variants, Incident Proteinuria, and Subsequent eGFR Decline in Blacks with Hypertension-Attributed CKD. Clin J Am Soc Nephrol 12:1771-1777

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