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HD Lighthouse Editor's Comment: It takes a while for medical practice to benefit from modern research. The HDSA recommends haloperidol for the treatment HD and widely distributes the outdated Physicians Guide to the Treatment of Huntington's Disease.
Because both the expanded HD gene and haloperidol decrease BDNF, a critical brain factor, it is likely haloperidol will accelerate the progression of HD. The side effects of haloperidol cruelly mimic HD and are often irreversible. The following research suggests safe alternatives for haloperidol that may go beyond symptomatic treatment and delay HD by up regulating BDNF. --Jerry
Expression of brain-derived neurotrophic factor mRNA in rat hippocampus after treatment with antipsychotic drugs.Typical and atypical antipsychotic drugs, though both effective, act on different neurotransmitter receptors and are dissimilar in some clinical effects and side effects. The typical antipsychotic drug haloperidol has been shown to cause a decrease in the expression of brain-derived neurotrophic factor (BDNF), which plays an important role in neuronal cell survival, differentiation, and neuronal connectivity. However, it is still unknown whether atypical antipsychotic drugs similarly regulate BDNF expression. We examined the effects of chronic (28 days) administration of typical and atypical antipsychotic drugs on BDNF mRNA expression in the rat hippocampus using in situ hybridization. Quantitative analysis revealed that the typical antipsychotic drug haloperidol (1 mg/kg) down-regulated BDNF mRNA expression in both CA1 (P < 0.05) and dentate gyrus (P < 0.01) regions compared with vehicle control. In contrast, the atypical antipsychotic agents clozapine (10 mg/kg) and olanzapine (2.7 mg/kg) up-regulated BDNF mRNA expression in CA1, CA3, and dentate gyrus regions of the rat hippocampus compared with their respective controls (P < 0.01). These findings demonstrate that the typical and atypical antipsychotic drugs differentially regulate BDNF mRNA expression in rat hippocampus. Source: J Neurosci Res 2003 Jan 1;71(1):127-31
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