The Role of Dopamine in Huntington’s Disease
Identifieur interne : 000049 ( Main/Exploration ); précédent : 000048; suivant : 000050The Role of Dopamine in Huntington’s Disease
Auteurs : Carlos Cepeda [États-Unis] ; Kerry P. S. Murphy [Royaume-Uni] ; Martin Parent [Canada] ; Michael S. Levine [États-Unis]Source :
- Progress in brain research [ 0079-6123 ] ; 2014.
Abstract
Alterations in dopamine (DA) neurotransmission in Parkinson’s disease are well-known and widely studied. Much less is known about DA changes that accompany and underlie some of the symptoms of Huntington’s disease (HD), a dominant inherited neurodegenerative disorder characterized by chorea, cognitive deficits and psychiatric disturbances. The cause is an expansion in CAG (glutamine) repeats in the
Url:
DOI: 10.1016/B978-0-444-63425-2.00010-6
PubMed: 24968783
PubMed Central: 4409123
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">Alterations in dopamine (DA) neurotransmission in Parkinson’s disease are well-known and widely studied. Much less is known about DA changes that accompany and underlie some of the symptoms of Huntington’s disease (HD), a dominant inherited neurodegenerative disorder characterized by chorea, cognitive deficits and psychiatric disturbances. The cause is an expansion in CAG (glutamine) repeats in the <italic>HTT</italic>
gene. The principal histopathology of HD is the loss of medium-sized spiny neurons (MSNs) and, to a lesser degree, neuronal loss in cerebral cortex, thalamus, hippocampus and hypothalamus. Neurochemical, electrophysiological and behavioral studies in HD patients and genetic mouse models suggest biphasic changes in DA neurotransmission. In the early stages DA neurotransmission is increased leading to hyperkinetic movements that can be alleviated by depleting DA stores. In contrast, in the late stages DA deficits produce hypokinesia that can be treated by increasing DA function. Alterations in DA neurotransmission affect glutamate receptor modulation and could contribute to excitotoxicity. The mechanisms of DA dysfunction, in particular the increased DA tone in the early stages of the disease, are presently unknown but may include initial upregulation of DA neuron activity caused by the genetic mutation, reduced inhibition resulting from striatal MSN loss, increased excitation from cortical inputs, and DA autoreceptor dysfunction. Targeting both DA and glutamate receptor dysfunction could be the best strategy to treat HD symptoms.</p>
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