Effects of idebenone on electroencephalograms of patients with cerebrovascular disorders

Nakano, Takashi; Miyasaka, Makoto; Mori, Katsumi; Ohtaka, Tadashi; Kifune, Yoshihisa

doi:10.1016/0167-4943(89)90016-2

Cited by 6 publications

(3 citation statements)

References 4 publications

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“…The present study was designed to evaluate the effect of WEB 1881 FU on hypoglycemic/ hypoxic brain injury, as compared to findings with idebenone, a cerebral metabolic en hancer (12,13), using an in vitro model that we have designed (14). g were housed in an air-conditioned room at 23±2'C with free access to food and water and main tained on a 12 hr light-dark schedule (lights on 7:00 a.m.).…”

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confidence: 99%

Evaluation of the Neuroprotective Action of WEB 1881 FU on Hypoglycemia/Hypoxia-Induced Neuronal Damage Using Rat Striatal Slices

Koizumi

Kataoka

Shigematsu

et al. 1990

Japanese Journal of Pharmacology

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Abstract-Effect of WEB 1881 FU on hypoglycemia/hypoxia-induced brain damage in rats was evaluated and compared to findings obtained with idebenone. We used an in vitro model that facilitated the direct monitoring of dopamine release from striatal slices. The response to high K+ stimulation under perfusion of the slices with D-glucose-free Ringer solution (hypoglycemia) decreased at 40 min, and then practically disappeared. WEB 1881 FU at 10-6 M or idebenone at 10-6 M significantly protected against impairment of the striatal responses under the con ditions of hypoglycemia. Hypoglycemic injury, evidenced by a remarkable neuron loss, necrosis and spongyosis was also ameliorated by these drugs. WEB 1881 FU at 10-6 M had a protective action against the impairment of striatal responses evoked by NaCN (electron transport inhibitor at site 3) and oligomycin (inhibitor of mito chondrial ATP synthesis), but idebenone at 10-6 M did not. In light of these obser vations, the possibility that WEB 1881 FU and idebenone exert neuroprotective actions against hypoglycemic/hypoxic brain injury by activating energy me tabolism with different mechanisms from each other has to be considered.

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confidence: 99%

Evaluation of the Neuroprotective Action of WEB 1881 FU on Hypoglycemia/Hypoxia-Induced Neuronal Damage Using Rat Striatal Slices

Koizumi

Kataoka

Shigematsu

et al. 1990

Japanese Journal of Pharmacology

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“…Препарат демонстрирует высокую степень безопасности и хорошую переносимость [39][40][41]. Безопасность и переносимость идебенона были сопоставимы с плацебо в ходе двухлетнего исследования с использованием дозы до 360 мг в день [39].…”

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Pathophysiological features of chronic cerebrovascular diseases and possibilities of complex neuroprotective therapy

Костенко

Петрова

2019

Med. sov.

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The article discusses the principles of neuroprotective therapy as a pathogenetically justified direction in chronic cerebrovascular diseases (CVD). The results of numerous clinical trials demonstrated efficacy, safety, a wide range of pharmacological effects and good tolerability of the powerful antioxidant Idebenone (Neyromet), as well as domestic cytoprotector, Choline alphosceratus of (Cerepro®), affecting the basic pathophysiological processes of the ischemic cascade at CVD. The role of rational multimodal pharmacotherapy of CVD, which provides the necessary energy for the processes of neuroprotection and neuroplasticity of brain cells, is emphasized.

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“…But it is in the 80s that various other classes of drugs considered active on the cerebrovascular disorders were introduced and proposed for clinical use. The first group was composed by the antioxidants pyritinol (Tazaki et al, 1980) and idebenone (Nakano et al, 1989) and was followed by a group including different vitamins, acetilcarnitine (Testa et al, International Psychogeriatrics, 15(Suppl. 1), 2003 1982) and folic acid (folates) (Fioravanti et al, 1997) and a group of compounds active on the phospholipid synthesis, cdp-choline (Agnoli et al, 1985) and alpha-glycerylphosphorylcholine (Di Perri, 1991).…”

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confidence: 99%

History of Symptomatic Therapy in Vascular Dementia

Fioravanti

2003

Int. Psychogeriatr.

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The therapy for vascular dementia has known several changes and updates since the use of niacin in the first years of the 20th century. These modifications were due to the parallel evolution of the concept of vascular dementia. Initially, treatments in this area were proposed because they were considered vasoactive and able to increase the blood flow of the brain. After these, other drugs were introduced because they were also able to ameliorate the oxygen usage by the suffering neurons. The more recent therapeutic proposals were made for drugs active on the metabolic activities of the brain, or with hemorrheological or antioxidant properties. As a consequence, a large array of different pharmacological properties were considered in proposing the several different kinds of drugs as useful in vascular dementia patients. The most recent attempt in this field consists of evaluating the usefulness of traditional antidementia drugs (those with anticholinesterase action) in patients with a prevalence of cerebrovascular disorders.

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Effects of idebenone on electroencephalograms of patients with cerebrovascular disorders

Cited by 6 publications

References 4 publications

Evaluation of the Neuroprotective Action of WEB 1881 FU on Hypoglycemia/Hypoxia-Induced Neuronal Damage Using Rat Striatal Slices

Evaluation of the Neuroprotective Action of WEB 1881 FU on Hypoglycemia/Hypoxia-Induced Neuronal Damage Using Rat Striatal Slices

Pathophysiological features of chronic cerebrovascular diseases and possibilities of complex neuroprotective therapy

History of Symptomatic Therapy in Vascular Dementia

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