Ignite Creation Date:
2024-05-05 @ 4:51 PM
Last Modification Date:
2024-10-26 @ 9:25 AM
Study NCT ID:
NCT00328874
Status:
COMPLETED
Last Update Posted:
2020-01-10
First Post:
2006-05-21
Brief Title:
Study About Safety and Efficacy of Coenzyme Q10 in Progressive Supranuclear Palsy
Sponsor:
German Parkinson Study Group GPS
Organization:
German Parkinson Study Group GPS
Study Overview
Official Title:
Mono-center Prospective Double-blind Placebo-controlled Randomized Clinical Phase IIa Trial to Assess the Safety Tolerability and Immediate Biological Effects of Coenzyme Q10 - nanoQuinon in Progressive Supranuclear Palsy
Status:
COMPLETED
Status Verified Date:
2008-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Study hypothesis
A 6-week po treatment with 5 mgKg Coenzyme Q10 is safe and tolerableincreases the brains metabolism and ameliorates clinical symptoms in patients with PSP
A 6-week po treatment with 5 mgKg Coenzyme Q10 is safe and tolerableincreases the brains metabolism and ameliorates clinical symptoms in patients with PSP
Detailed Description:
Background and Rationale
1 Progressive Supranuclear Palsy PSP Steele-Richardson-Olszewski Syndrome is a sporadic neurodegenerative disorder resulting clinically in a Parkinson syndrome ie akinetic-rigid movement disorder with prominent postural instability oculomotor deficits and cognitive decline for review Albers and Augood 2001 Burn and Lees 2002 With an average annual incidence of 53 per 100000 and an age-adjusted prevalence of 64 per 100000 PSP is as common as motor-neuron disease Burn and Lees 2002 There is no symptomatic treatment because PSP patients do not respond to any known therapy Albers and Augood 2001 Burn and Lees 2002 The progression of PSP is rapid and the median survival after onset of symptoms is 5-10 years Albers and Augood 2001 Presently there is no known effective symptomatic or neuroprotective therapy for PSP
2 Evidence suggests an impairment of mitochondrial energy metabolism in PSP Albers and Beal 2002
1 Reduced cerebral glucose and ATP metabolism have been shown in functional imaging studies in PSP patients Forster et al 1988 Martinelli et al 2000
2 Cybrid cells harboring mitochondrial genes from PSP patients have decreased ATP-levels and complex I activity Swerdlow et al 2000 Albers et al 2001 Chirichigno et al 2002
3 A tropical PSP-like tauopathy has been linked clinically and experimentally to the consumption of the fruit and teas of leaves of the tropical plant annona muricata rich in lipophilic complex I inhibitors Caparros-Lefebvre et al 1999 2001 These clinical observations suggest a role for mitochondrial dysfunction in the etiology of PSP
3Coenzyme Q10 CoQ10 is the physiological electron recipient of complex I Exogenous CoQ10 1 enhances the electron transport by complex I and 2 powerfully scavenges free radicals Thus CoQ10 has been shown to reduce the toxicity of complex I inhibitors in vitro Menke et al 2003 and in vivo Beal et al 1998
1 Progressive Supranuclear Palsy PSP Steele-Richardson-Olszewski Syndrome is a sporadic neurodegenerative disorder resulting clinically in a Parkinson syndrome ie akinetic-rigid movement disorder with prominent postural instability oculomotor deficits and cognitive decline for review Albers and Augood 2001 Burn and Lees 2002 With an average annual incidence of 53 per 100000 and an age-adjusted prevalence of 64 per 100000 PSP is as common as motor-neuron disease Burn and Lees 2002 There is no symptomatic treatment because PSP patients do not respond to any known therapy Albers and Augood 2001 Burn and Lees 2002 The progression of PSP is rapid and the median survival after onset of symptoms is 5-10 years Albers and Augood 2001 Presently there is no known effective symptomatic or neuroprotective therapy for PSP
2 Evidence suggests an impairment of mitochondrial energy metabolism in PSP Albers and Beal 2002
1 Reduced cerebral glucose and ATP metabolism have been shown in functional imaging studies in PSP patients Forster et al 1988 Martinelli et al 2000
2 Cybrid cells harboring mitochondrial genes from PSP patients have decreased ATP-levels and complex I activity Swerdlow et al 2000 Albers et al 2001 Chirichigno et al 2002
3 A tropical PSP-like tauopathy has been linked clinically and experimentally to the consumption of the fruit and teas of leaves of the tropical plant annona muricata rich in lipophilic complex I inhibitors Caparros-Lefebvre et al 1999 2001 These clinical observations suggest a role for mitochondrial dysfunction in the etiology of PSP
3Coenzyme Q10 CoQ10 is the physiological electron recipient of complex I Exogenous CoQ10 1 enhances the electron transport by complex I and 2 powerfully scavenges free radicals Thus CoQ10 has been shown to reduce the toxicity of complex I inhibitors in vitro Menke et al 2003 and in vivo Beal et al 1998
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None