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2000
Volume 22, Issue 14
  • ISSN: 1570-159X
  • E-ISSN: 1875-6190

Abstract

Background

Excessive free radicals are implicated in the pathophysiology of tardive dyskinesia (TD), and extract (EGb761) scavenges free radicals, thereby enhancing antioxidant enzymes such as mitochondrial manganese superoxide dismutase (). This study examined whether EGb761 treatment would improve TD symptoms and increase activity, particularly in TD patients with specific Val-9Ala genotype.

Methods

An EGb761 (240 mg/day) 12-week double-blind clinical trial with 157 TD patients was randomized. The severity of TD was measured by the Abnormal Involuntary Movement Scale (AIMS) and plasma activity was assayed before and after 12 weeks of treatment. Further, in an expanded sample, we compared activity in 159 TD, 227 non-TD and 280 healthy controls, as well as the allele frequencies and genotypes for the Ala-9Val polymorphism in 352 TD, 486 non-TD and 1150 healthy controls.

Results

EGb761 significantly reduced TD symptoms and increased activity in TD patients compared to placebo (both < 0.01). Moreover, we found an interaction between genotype and treatment response ( < 0.001). Furthermore, in the EGb761 group, patients carrying the Ala allele displayed a significantly lower AIMS total score than patients with the Val/Val genotype. In addition, activity was significantly lower at baseline in TD patients compared with healthy controls or non-TD patients.

Conclusion

EGb761 treatment enhanced low activity in TD patients and produced greater improvement in TD symptoms in patients with the Ala allele of the Ala-9Val polymorphism.

Clinical Trial Registration No

NCT00672373.

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2024-12-01
2024-11-26
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