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Idebenone improves
learning and memory impairment induced by cholinergic or serotonergic
dysfunction in rats.
Yamazaki N, Nomura M, Nagaoka A, Nagawa Y.
Central Research Division,
Takeda Chemical Industries, Ltd., Osaka, Japan.
Arch Gerontol Geriatr 1989 May;8(3):225-39
ABSTRACT
The effects of idebenone, a
cerebral metabolic enhancer, on learning and memory impairment in two rat
models with central cholinergic or serotonergic dysfunction were investigated
using positively reinforced learning tasks. A delayed alternation task using a
T maze was employed to test the effect of idebenone on short-term memory
impairment induced by a cholinergic antagonist, scopolamine. A correct
response, defined as a turn toward the arm opposite to that in the forced run,
was rewarded with food pellets. Scopolamine (0.2 and 0.5 mg/kg, i.p.)
significantly decreased the correct responses to the chance level in the
60-s-delayed alternation task. The scopolamine (0.2 mg/kg, i.p.)-induced
impairment of short-term memory was improved by idebenone (3-30 mg/kg, i.p.)
or an acetylcholinesterase inhibitor, physostigmine (0.1 and 0.2 mg/kg, i.p.),
administered simultaneously. The central serotonergic dysfunction model was
produced by giving rats a diet deficient in tryptophan, a precursor of
serotonin. The rats fed on a tryptophan-deficient diet (TDD) showed a slower
learning process in the operant brightness discrimination task (mult V115 EXT)
than did rats fed on a normal diet. Idebenone (60 mg/kg/day) admixed with the
TDD decreased the number of lever-pressing responses emitted during the
extinction periods. The percentage of correct responses was significantly
higher in the idebenone-treated group than in the control TDD group. These
results suggest that idebenone may improve both the impairment of short-term
memory induced by a decreased cholinergic activity and the retardation of
discrimination learning induced by central serotonergic dysfunction.
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Cardiomyopathy
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improvement in mitochondrial cardiomyopathy following
treatment with idebenone
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Leber hereditary optic neuropathy (LHON)
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does it shorten the time to visual recovery in Leber hereditary optic
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improvement in a patient with Leber's hereditary optic neuropathy (LHON)
Misc.
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use in age-related cognitive disorders
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protects hippocampal neurons against beta amyloid neurotoxicity
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functions as a potent protective
hepatocyte antioxidant
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neuroprotective effects of
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inhibition of brain mitochondrial
swelling
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suppression of cold ischemia/reperfusion
injury of liver endothelium
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ability to eliminate a nitroxide
radical in the rat
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interaction with respiratory complexes of heart
mitochondria
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effect on serotonin release and seroton receptors in
rats
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protects hepatic microsomes against damage in organ preservation solutions
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protects against toxicity
induced by low density lipoprotein
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protects against disorders due to cerebral hypoxia or
ischemia
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protects against toxicity induced by low density
lipoprotein
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attenuates neuronal degeneration induced by excitotoxins
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augments long-term potentiation in
hippocampal slices in the guinea pig
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on lipid peroxidation
in erythrocytes of stroke-prone, hypertensive rats
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brain distribution and its effect on local cerebral
glucose utilization in rats
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effects
on acetylcholine
levels in the brains of rats with cerebral ischemia
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protective effect of idebenone against hypoxia in mice
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improves learning and memory impairment induced in rats
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effects
of idebenone on
neurological deficits in stroke-prone rats
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effects
on memory induced impairment in rats
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effects of idebenone on cerebral blood flow in rats with cerebral ischemia
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inhibition
of brain mitochondrial swelling by idebenone
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inhibition of platelet aggregation
by idebenone
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effects of idebenone on monoamine metabolites of
patients with dementia
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effects of idebenone on
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on impairment of radial maze learning in cerebral embolized rats
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effect of idebenone on lipid peroxidation in rat
brain homogenate
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effects on muricidal behavior in rats with raphe
lesions
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inhibitory effect of idebenone on vascular lesions in
hypertensive rats
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