NCT00331812|Unknown
Mitochondrial Functions and Oxidative Stress in ALS Patients
Study of Mitochondrial Functions and Oxidative Stress in ALS Patients.
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Study of Mitochondrial Functions and Oxidative Stress in ALS Patients.
Sponsor study identifier
observational
40
1 country
1
Study Start
February 2006
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
Not reported
Date not reportedStudy Completion
February 2008
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
In Amyotrophic Lateral Sclerosis (ALS), malnutrition is frequent (16 to 50 % of the patients) and is an independent prognostic factor. One of the implicated factors is the increase of resting energy expenditure (REE) which can be found in about 50 % of ALS patients. The origin of this hypermetabolism is currently unknown but could be located in the mitochondria. In fact, some studies have found mitochondrial abnormalities and the existence of an oxidative stress. Thus, the aim of this study is to characterize the mitochondrial abnormalities and the oxidant/antioxidant status of ALS patients and to determine their relationship with the metabolic status, hypermetabolism or normometabolism. Three groups of patients will be studied : 20 hypermetabolic ALS patients, 20 normometabolic ALS patients and 20 healthy volunteers paired for age and sex.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
February 2008
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
February 2006
Date type not reportedThis date has not been verified as actual or estimated.
May 23, 2006
Actual (reported)May 31, 2006
Actual (reported)February 2008
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
relationship between these abnormalities and the metabolic status (hypermetabolism or normometabolism).
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Three groups of patients will be studied : 20 hypermetabolic ALS patients, 20 normometabolic ALS patients and 20 healthy volunteers paired for age and sex.
Clermont-Ferrand University Hospital
Clermont-Ferrand, Auvergne, 63000, France
Desport JC, Preux PM, Magy L, Boirie Y, Vallat JM, Beaufrere B, Couratier P. Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis. Am J Clin Nutr. 2001 Sep;74(3):328-34. doi: 10.1093/ajcn/74.3.328.
Ferrante RJ, Browne SE, Shinobu LA, Bowling AC, Baik MJ, MacGarvey U, Kowall NW, Brown RH Jr, Beal MF. Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis. J Neurochem. 1997 Nov;69(5):2064-74. doi: 10.1046/j.1471-4159.1997.69052064.x.
Corinne Bouteloup, Dr
University Hospital, Clermont-Ferrand
First Submitted
May 23, 2006
First Posted
May 31, 2006
Study Start
February 2006
Date type not reportedThis date has not been verified as actual or estimated.
Study Completion
February 2008
Estimated (date passed)This estimate has passed. The registry has not confirmed an actual date for this milestone.
The Pre-symptomatic Familial Amyotrophic Lateral Sclerosis (Pre-fALS) Study
Contact the study team to confirm eligibility.
Menzies FM, Ince PG, Shaw PJ. Mitochondrial involvement in amyotrophic lateral sclerosis. Neurochem Int. 2002 May;40(6):543-51. doi: 10.1016/s0197-0186(01)00125-5.
Last Updated
January 19, 2011
Record last verified: 2011-01
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