کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2530678 | 1120468 | 2007 | 6 صفحه PDF | دانلود رایگان |
Huntington's disease (HD) is a late-onset neurodegenerative disorder that follows an autosomal-dominant pattern of inheritance. In human cases of HD and experimental models of the disease, multiple alterations in neurotransmitters and post-receptor machineries have been described. Dopamine, acetylcholine and glutamate signalling, which usually cooperate in the induction of physiological synaptic plasticity, are all disrupted. Impairment of the induction and reversal of the main forms of neuronal synaptic plasticity influences the computational function of complex neural circuits that mediate essential cognitive and motor functions. As long-term potentiation and long-term depression represent the accepted model for neuronal learning processes, their impairment could account for the onset and progression of both motor and cognitive symptoms of HD.
Journal: Current Opinion in Pharmacology - Volume 7, Issue 1, February 2007, Pages 106–111