Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases · 2000
Oral administration of creatine monohydrate retards progression of motor neuron disease in the wobbler mouse.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ikeda K, Iwasaki Y, Kinoshita M
Аннотация
BACKGROUND AND AIMS: Creatine has a neuroprotective effect in mutant superoxide dismutase (G93A) transgenic mice, an animal model of motor neuron disease (MND). Treatment with creatine monohydrate enhances muscle strength in patients with neuromuscular disorders. The purpose of our study was to determine whether administration of creatine monohydrate can attenuate progressive disease in wobbler mice.
METHODS: After an initial diagnosis of disease at the age of 3-4 weeks, creatine monohydrate (5 or 50 mg/kg, po) or vehicle was given to wobbler mice daily for 4 weeks in a blinded fashion. We compared symptomatic and neuropathological assessments among the three groups.
RESULTS: Creatine levels in biceps muscles were increased by approximately 20% following administration of higher-dose creatine monohydrate. In comparison with vehicle, treatment with higher doses of creatine monohydrate potentiated grip strength, attenuated forelimb contracture and increased the weight of biceps muscles. Mice treated with higher doses of creatine monohydrate showed retarded denervation muscle atrophy in the biceps muscles and reduced degeneration of the spinal motor neurons. Thus, oral administration of creatine monohydrate delayed the progression of disease in wobbler mice.
CONCLUSION: Our results indicate that this molecule may have therapeutic potential in human motor neuropathy or MND.
METHODS: After an initial diagnosis of disease at the age of 3-4 weeks, creatine monohydrate (5 or 50 mg/kg, po) or vehicle was given to wobbler mice daily for 4 weeks in a blinded fashion. We compared symptomatic and neuropathological assessments among the three groups.
RESULTS: Creatine levels in biceps muscles were increased by approximately 20% following administration of higher-dose creatine monohydrate. In comparison with vehicle, treatment with higher doses of creatine monohydrate potentiated grip strength, attenuated forelimb contracture and increased the weight of biceps muscles. Mice treated with higher doses of creatine monohydrate showed retarded denervation muscle atrophy in the biceps muscles and reduced degeneration of the spinal motor neurons. Thus, oral administration of creatine monohydrate delayed the progression of disease in wobbler mice.
CONCLUSION: Our results indicate that this molecule may have therapeutic potential in human motor neuropathy or MND.