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huntington disease/nikotin
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Neuroprotective effect of nicotine against 3-nitropropionic acid (3-NP)-induced experimental Huntington's disease in rats.
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Nicotinic acetylcholine receptors (nAChRs) are regarded as potential therapeutic targets to control various neurodegenerative diseases. Owing to the relevance of cholinergic neurotransmission in the pathogenesis of Huntington's disease (HD) this investigation was aimed to study the effect of
Nicotine potentiates the behavioral effects of haloperidol.
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Nicotine potentiates the catalepsy produced by haloperidol. Furthermore, nicotine as an adjunct to haloperidol produces a remarkable improvement in motor tics in Tourette's syndrome (TS) patients. The present experiments (1) compared the ability of nicotine to potentiate the catalepsy produced by
Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome.
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Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement
Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons.
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Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as
Endogenous sodium-potassium ATPase inhibition related biochemical cascade in trisomy 21 and Huntington's disease: neural regulation of genomic function.
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The isoprenoid pathway related cascade was assessed in trisomy 21 and Huntington's disease. Membrane Na+-K+ ATPase activity, serum magnesium and ubiquinone were decreased while HMG CoA reductase activity, serum digoxin and dolichol levels were increased in both the disorders. There were increased
Nicotine potentiates haloperidol-induced catalepsy and locomotor hypoactivity.
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Nicotine was found to potentiate the catalepsy and reduced locomotion following the administration of haloperidol. The ability of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) to potentiate the catalepsy produced by haloperidol (0.1, 0.2 or 0.4 mg/kg) was investigated. Nicotine potentiated the
Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.
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Maternal smoking during pregnancy is associated with low birth weight, increased risk of stillbirth, conduct disorder, attention-deficit/hyperactivity disorder and neurocognitive deficits. Ventral tegmental area dopamine (DA) neurons in the mesocorticolimbic pathway were suggested to play a critical
Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation.
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Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype
Substance abuse may be a risk factor for earlier onset of Huntington disease.
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Environmental factors may contribute as much as one-third of the variance in Huntington disease (HD) age of onset. Substance abuse is a risk factor for other neurodegenerative disorders; however, whether substance abuse influences HD age of onset is not well established. This study investigated the
Substance abuse may hasten motor onset of Huntington disease: Evaluating the Enroll-HD database.
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OBJECTIVE
To investigate the relationship between substances of abuse and age at motor onset (AMO) in patients with Huntington disease (HD) in a large and diverse patient population.
METHODS
This was a retrospective, observational study of the Enroll-HD database. Participants were determined to
Factors associated with slow progression in Huntington's disease.
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The rate of disease progression was assessed for 42 persons affected by Huntington's disease who had been neurologically examined at least six times and followed up for at least 3 years. Disease progression was assessed by a disability rating scale administered at each examination. Slow progression
Cholinergic receptors in cognitive disorders.
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Cholinergic receptors (muscarinic subtypes M1 and M2, and putative nicotinic binding) have been examined in the hippocampus obtained at autopsy from a variety of patients with cognitive disorders (Alzheimer's, Parkinson's, and Huntington's diseases, Down's Syndrome and alcoholic dementia) and
Nicotinic receptor modulation for neuroprotection and enhancement of functional recovery following brain injury or disease.
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Despite the well-known adverse health effects of tobacco smoking, numerous studies have shown that nicotine, the principal pharmacologically active alkaloid in tobacco smoke, exerts neuroprotective properties in several animal models of neurodegeneration. Furthermore, cigarette smoking appears to
Evidence for the use of "medical marijuana" in psychiatric and neurologic disorders.
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UNASSIGNED
Cannabis is listed as a Schedule I substance under the Controlled Substances Act of 1970, meaning the US federal government defines it as an illegal drug that has high potential for abuse and no established medical use; however, half of the states in the nation have enacted "medical
[Kynurenine and its metabolites in nervous system diseases].
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Kynurenine is a metabolite of the tryptophan-nicotine-amide-adenine-dinucleotide pathway. Recent preclinical and clinical data suggest that kynurenine and its metabolites (kynurenic acid, quinolinic acid) may play important role in the pathogenesis of neurological and other disorders (Huntington's
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