Creatine supplementation in Parkinson disease: A placebo-controlled randomized pilot trial

Bender, Andreas; Koch, Walter; Elstner, Matthias; Schombacher, Y.; Bender, Julia Lynne Glade; Moeschl, M.; Gekeler, Florian; Müller‐Myhsok, Bertram; Gasser, Thomas; Tatsch, Klaus; Klopstock, Thomas

doi:10.1212/01.wnl.0000238518.34389.12

Cited by 175 publications

(119 citation statements)

References 10 publications

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“…91 Another blinded, placebocontrolled study of 2 g daily for 6 months then 4 g daily for 18 months in 31 PD patients compared with 17 placebo showed no significant differences compared with placebo. 92 An antiapoptotic agent, TCH346, did not demonstrate neuroprotection in early PD patients. 93 Rasagiline, a monoamine oxidase B inhibitor, has demonstrated benefit in a delayedstart study in early PD that may reflect modification of the progression of the disease over the period of study (18 months).…”

Section: Therapeutic Implicationsmentioning

confidence: 94%

Mitochondrial Pathology in Parkinson's Disease

Schapira

2011

Mount Sinai J Medicine

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The last 25 years have witnessed remarkable advances in our understanding of the etiology and pathogenesis of Parkinson's disease. The ability to undertake detailed biochemical analyses of the Parkinson's disease postmortem brain enabled the identification of defects of mitochondrial and free‐radical metabolism. The discovery of the first gene mutation for Parkinson's disease, in alpha‐synuclein, ushered in the genetic era for the disease and the subsequent finding of several gene mutations causing parkinsonism, 15 at the time of writing. Technological advances both in sequencing technology and software analysis have allowed association studies of sufficiently large size accurately to describe genes conferring an increased risk for Parkinson's disease. What has been so surprising is the convergence of these 2 separate disciplines (biochemistry and genetics) in terms of reinforcing the importance of the same pathways (ie, mitochondrial dysfunction and free‐radical metabolism). Other pathways are also important in pathogenesis, including protein turnover, inflammation, and post‐translational modification, particularly protein phosphorylation and ubiquitination. However, even these additional pathways overlap with each other and with those of mitochondrial dysfunction and oxidative stress. This review explores these concepts with particular relevance to mitochondrial involvement. Mt Sinai J Med 78:872–881, 2011. © 2011 Mount Sinai School of Medicine

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Section: Therapeutic Implicationsmentioning

confidence: 94%

Mitochondrial Pathology in Parkinson's Disease

Schapira

2011

Mount Sinai J Medicine

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“…Creatine also improved brain bioenergetics in a dose-ranging 31 P MRS study of adolescent females with drug-resistant depression (Kondo et al 2016). Yet, several clinical studies reported low-to-medium therapeutic potential of creatine to positively dysfunctional energy metabolism in Huntington's disease (Bender et al 2005) and Parkinson's disease (Bender et al 2006), also schizophrenia (Kaptsan et al 2007). Co-administration of creatine and ketogenic diet did not result in 31 P-MRS visible changes in muscle energy metabolism in patients with McArdle disease although the intervention showed some energy-independent beneficial effects (Vorgerd and Zange 2007).…”

Section: Tackling Impaired Bioenergeticsmentioning

confidence: 99%

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Ostojić

2017

Tohoku J. Exp. Med.

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Mitochondrial energy deficit is considered a key element of different clinical pathologies -from inherited disorders of energy metabolism to drug-induced mitochondrial toxicity, to cardiometabolic and neurodegenerative diseases. However, clinical manifestations of impaired bioenergetics are not easy to recognize, with patient-reported features usually include non-pathognomonic fatigue and weakness, or exercise intolerance, while specific lab tests are missing. Although it is not clear whether poor energetics is a primary deficit or a secondary consequence of specific disorders, improving mitochondrial viability remains a challenging task in both experimental and clinical medicine. In this review, biochemical and clinical evidence of energy deficits were reviewed, along with possible therapeutic options to tackle energy failure and restore bioenergetics.

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“…88 Another placebo-controlled study evaluating creatine supplementation was conducted in 60 subjects. 89 This study differed from the NET-PD trial in that subjects were receiving levodopa and other anti-parkinsonian therapy (except for selegiline). The assessment of change over the 2-year study was made by comparing clinical ratings while subjects were receiving the same dosages of PD medications at the end of the study as were taken initially.…”

Section: Creatinementioning

confidence: 99%

Protection Against Parkinson’s Disease Progression: Clinical Experience

LeWitt

Taylor

2008

Neurotherapeutics

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Summary:Treatments with potential neuroprotective capability for Parkinson's disease (PD) have been investigated in randomized, controlled, clinical trials and other studies since the mid-1980s. Although promising leads have arisen, no therapy has been proven to halt or slow disease progression. Several large-scale studies have highlighted progress in methodology, as well as the frustrations of translating laboratory science to practical applications. This review summarizes findings from clinical trials with several classes of compounds, including monoamine oxidase-B inhibitors (selegiline, lazabemide, rasagiline), dopaminergic drugs (ropinirole, pramipexole, levodopa), antioxidant strategies (␣-tocopherol), mitochondrial energy enhancers (coenzyme Q 10 , creatine), antiapoptotic agents (TCH346, minocycline, CEP-1347), and antiglutamatergic compounds (riluzole). Beyond small-molecule pharmacology, gene therapy approaches, such as delivering neurotrophic substances (e.g., neurturin) by viral vector, are the next generation of treatment options.

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Creatine supplementation in Parkinson disease: A placebo-controlled randomized pilot trial

Cited by 175 publications

References 10 publications

Mitochondrial Pathology in Parkinson's Disease

Mitochondrial Pathology in Parkinson's Disease

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Protection Against Parkinson’s Disease Progression: Clinical Experience

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