Pramipexole reverses Parkinson's disease‐related motivational deficits in rats

Favier, Marc; Duran, Théo; Carcenac, Carole; Drui, Guillaume; Savasta, Marc; Carnicella, Sébastien

doi:10.1002/mds.25837

Cited by 52 publications

(58 citation statements)

References 57 publications

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“…This (Favier et al, 2014;Schulte-Herbruggen et al, 2012;Siuciak and Fujiwara, 2004) and in clinical trials alone (Barone et al, 2010) or in combination with L-DOPA (Rektorova et al, 2005). In autoradiography studies PPX binding was shown to be high also in mesolimbic areas like the nucleus accumbens, olfactory tubercle and amygdala.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 95%

Long-term treatment with l-DOPA or pramipexole affects adult neurogenesis and corresponding non-motor behavior in a mouse model of Parkinson's disease

et al. 2015

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 95%

Long-term treatment with l-DOPA or pramipexole affects adult neurogenesis and corresponding non-motor behavior in a mouse model of Parkinson's disease

et al. 2015

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“…A more widespread degeneration of mesocortical, mesolimbic, and mesostriatal dopaminergic projections, originating in the ventral tegmental area and SNc, is likely to be involved in motivational and affective manifestations of PD . Dopaminergic involvement in neuropsychiatric NMF has been supported by several studies that demonstrate mood changes related to l ‐dopa infusion in a dose‐dependent fashion and dopamine modulation of cognitive functions in nondemented PD patients .…”

Section: Neuropsychiatric Fluctuationsmentioning

confidence: 95%

The hidden sister of motor fluctuations in Parkinson's disease: A review on nonmotor fluctuations

et al. 2016

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Only a few years after the introduction of levodopa, the first descriptions of motor fluctuations and dyskinesia related to dopaminergic therapy appeared. In PD, attention turned to their management, that had dampened the euphoria of the “levodopa miracle.” It soon became clear that neuropsychiatric, autonomic, and sensory features also tend to develop fluctuations after chronic exposure to l‐dopa. The diversity of fluctuating nonmotor symptoms, their largely subjective nature, coupled with a frequent lack of insight led to difficulties in identification and quantification. This may explain why, despite the high impact of nonmotor symptoms on patient autonomy and quality of life, evaluation of nonmotor fluctuations is not part of clinical routine. In view of the lack of specific validated assessment tools, detailed anamnesis should ideally be coupled with an evaluation in both ON and OFF drug conditions. The mechanisms of nonmotor fluctuations are not well understood. It is thought that they share dopaminergic presynaptic pharmacokinetic and postsynaptic pharmacodynamic mechanisms with the classical motor complications, but involve different neural pathways. Although symptoms fluctuate with dopaminergic treatment, serotonine and norepinephrine denervation, as well as interactions between neurotransmitter systems, probably contribute to their diversity. The lack of validated tools for assessment of these phenomena explains the almost complete absence of treatment studies. Management, largely resulting from expert opinion, includes psychiatric follow‐up, nondopaminergic drugs, and advanced dopaminergic treatment, including drug delivery pumps and DBS. This review aims to provide a starting point for the understanding, diagnosis, and management of nonmotor fluctuations. © 2016 International Parkinson and Movement Disorder Society

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“…Apathy occurring during premotor PD can account for the typical premorbid parkinsonian personality of reduced sensation seeking, reduced smoking, and lower alcohol and caffeine intake. Apathy can be seen as the nonmotor emotional counterpart of akinesia.…”

Section: Hypodopaminergic Behavioral Syndromementioning

confidence: 99%

Emotional manifestations of PD: Neurobiological basis

et al. 2016

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Neuropsychiatric symptoms are common and disabling in PD. Their neurobiological bases are complex, partly because of the disease itself and partly because of the dopaminergic treatment. The aim of this review is to focus on the emotional manifestations stemming from the neurodegenerative process itself. We focus on depression, anxiety, apathy, and fatigue, which can all be part of the clinical spectrum of premotor disease and may be improved or masked by medications targeting parkinsonian motor signs or psychiatric symptoms as the disease progresses. Findings from clinical, neuroimaging, and animal studies are reviewed, showing a major contribution of the dopaminergic system to the pathophysiology of these disabling symptoms. Degeneration of noradrenergic and serotonergic projection systems also has an impact on psychiatric symptoms of PD. The available literature is reviewed, but at present there is a lack of studies that would allow disentangling the separate contribution of each of the monoaminergic systems. The use of a pragmatic classification of all these symptoms under the umbrella of hypodopaminergic behavioral syndrome seems clinically useful, as it emphasizes the crucial, although not exclusive, nature of their dopaminergic neurobiological basis, which has important implications in the clinical management of PD. Psychiatric symptoms are so common in Parkinson's disease (PD) that it has been defined as a neuropsychiatric disorder.1 Neuropsychiatric symptoms, that is, emotional and cognitive symptoms, constitute a major source of disability and can be socially disruptive. [2][3][4] Some of these symptoms are a side effect of dopaminergic treatment (behavioral and dopaminergic replacement treatment addiction, nocturnal hyperactivity, hypomania, and punding).3-5 Others, like apathy, depression, and anxiety, seem more related to the disease itself, already presenting in the early stages of the disease and potentially preceding the first motor symptoms. As such, apathy, depression, and anxiety might at least in part be associated with insufficient dopaminergic drive. [4][5][6][7][8] Fluctuating patients might experience apathy, depression, and anxiety in the offperiods, with euphoria, well-being, self-confidence, and hypomania characterizing the on-drug condition. 9 The management of neuropsychiatric symptoms remains a challenge, also because it is not always easy to weight the relative contribution of medications, disease, and emotional response. The neurobiological bases of these symptoms are complex and not yet fully understood. The relative contribution of dopaminergic deficit and of other nondopaminergic systems is still under investigation. The objective of this review is to focus on the neuropsychiatric symptoms, which are most likely related to the disease itself, and to analyze ------------------------------------------------------------ N O N M O T O R S E R I E S : R E V I E WMovement Disorders, Vol. 31, No. 8, 2016 1103 the literature relating to their underlying mechanisms. We will...

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Pramipexole reverses Parkinson's disease‐related motivational deficits in rats

Cited by 52 publications

References 57 publications

Long-term treatment with l-DOPA or pramipexole affects adult neurogenesis and corresponding non-motor behavior in a mouse model of Parkinson's disease

Long-term treatment with l-DOPA or pramipexole affects adult neurogenesis and corresponding non-motor behavior in a mouse model of Parkinson's disease

The hidden sister of motor fluctuations in Parkinson's disease: A review on nonmotor fluctuations

Emotional manifestations of PD: Neurobiological basis

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