Neurodegenerative movement disorders: the contribution of functional imaging

Piccini, Paola

doi:10.1097/01.wco.0000137538.84115.3c

Cited by 21 publications

(13 citation statements)

References 70 publications

(43 reference statements)

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“…For instance, the relative concentration of D1-like receptors compared to D2 receptor is higher in the prefrontal cortex, whereas the concentration of D2-like receptors is elevated in the caudate nucleus, putamen, and nucleus accumbens [26,29]. Importantly, although D1 and D2 receptors have opposite effect at the molecular level, they often act synergistically when more complex outputs are taken into account [30,31]. …”

Section: The Mesocorticolimbic Dopamine Systemmentioning

confidence: 99%

Dopaminergic reward system: a short integrative review

Arias-Carrión¹,

Stamelou²,

et al. 2010

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Memory is an essential element to adaptive behavior since it allows consolidation of past experience guiding the subject to consider them in future experiences. Among the endogenous molecules that participate in the consolidation of memory, including the drug-seeking reward, considered as a form of learning, is dopamine. This neurotransmitter modulates the activity of specific brain nucleus such as nuclei accumbens, putamen, ventral tegmental area (VTA), among others and synchronizes the activity of these nuclei to establish the neurobiological mechanism to set the hedonic element of learning. We review the experimental evidence that highlights the activity of different brain nuclei modulating the mechanisms whereby dopamine biases memory towards events that are of motivational significance.

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Section: The Mesocorticolimbic Dopamine Systemmentioning

confidence: 99%

Dopaminergic reward system: a short integrative review

Arias-Carrión¹,

Stamelou²,

et al. 2010

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“…C-raclopride PET studies in the brains of living and symptomatic human HD patients indicate reduced dopamine receptor labeling is correlated with disease progression, cell loss and cognitive impairment [137]. Importantly, reduced dopamine-receptor binding is also prominent in the striatum and cortex of presymptomatic HD gene carriers, indicating dopamine dysfunction to be onboard before clinical manifestation of the disease [137]. Mirroring human HD, reduced dopamine D 2 -receptor binding is also evident in KI HD mice before HD phenotypic expression [138].…”

Section: Aberrant Dopaminergic Signaling In the Huntington’s Disease mentioning

confidence: 99%

Corticostriatal circuit dysfunction in Huntington‘s disease: intersection of glutamate, dopamine and calcium

Miller

Bezprozvanny²

2010

Future Neurol.

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Huntington’s disease (HD) is a noncurable and progressive autosomal-dominant neurodegenerative disorder that results from a polyglutamine expansion in the amino-terminal region of the huntingtin protein. The generation of rodent HD models has revealed that cellular dysfunction, rather than cell death alone, occurs early in the disease progression, appearing even before overt symptom onset. Much evidence has now established that dysfunction of the corticostriatal circuit is key to HD symptomology. In this article, we summarize the most current findings that implicate glutamate, dopamine and calcium signaling in this system and discuss how they work in concert to disrupt corticostriatal function. In addition, we highlight therapeutic strategies related to altered corticostriatal signaling in HD.

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“…Positron‐emission tomography studies assessing PD patients with D2 receptor ligands, such as [ 11 C]‐Raclopride showed a mild increase in D2 site availability in the putamen [34]. PET [ 18 F]‐DOPA studies have also shown an increase of the AADC activity outside the striatum, especially, in the anterior cingulated and prefrontal cortex.…”

Section: Molecular Imaging Of Spd (Non‐genetic‐linked Parkinsonism)mentioning

confidence: 99%

Molecular imaging in hereditary forms of parkinsonism

Shih

Felı́cio

Godeiro-Júnior

et al. 2007

Euro J of Neurology

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The development of in vivo molecular imaging to evaluate the dopamine (DA) system with positron-emission tomography and single photon emission computed tomography has been of key importance on monitoring in vivo nigrostriatal neuronal loss in Parkinson's disease (PD), mostly through assessments of pre- and post-synaptic DA receptors. The discoveries of genes related to hereditary forms of parkinsonism (PARK1, PARK2, PARK6, PARK7 and PARK8) have increased our understanding either of distinct subtypes of clinical expression in PD or its etiology. This article revises current data on molecular neuroimaging of genetic forms of parkinsonism comparing and contrasting its main features with the classical sporadic forms. Awareness of the spectrum variance in the genotype and its respective PD phenotype are useful to distinguish different pathophysiological mechanisms of PD.

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Neurodegenerative movement disorders: the contribution of functional imaging

Cited by 21 publications

References 70 publications

Dopaminergic reward system: a short integrative review

Dopaminergic reward system: a short integrative review

Corticostriatal circuit dysfunction in Huntington‘s disease: intersection of glutamate, dopamine and calcium

Molecular imaging in hereditary forms of parkinsonism

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