Circadian Determinations of Cortisol, Prolactin and Melatonin in Chronic Methyl-Phenyl-Tetrahydropyridine-Treated Monkeys

Barcia, Carlos; Mora-Bautista, Víctor Manuel; Sánchez-Bahillo, Ángel; Fernández-Villalba, Emiliano; Navarro-Ruis, Juana-María; Barreiro, Anabela; Poza, Máximo; Herrero, M.T.

doi:10.1159/000071967

Cited by 34 publications

(23 citation statements)

References 29 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…First, dopamine is implicated in circadian mechanisms including the light input and adaptation in the retina [102,103] and the regulation of specific hormones, such as cortisol, prolactin, and melatonin [104]. The interaction between dopamine and melatonin [105], a major regulator of the circadian rhythm, seems to be closely linked to Parkinson's disease progression [106,107].…”

Section: Sleep-wake Neurobiology In Prodromal Parkinson's Diseasementioning

confidence: 99%

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

Bargiotas

Schuepbach

Bassetti

2016

Current Opinion in Neurology

View full text Add to dashboard Cite

Purpose of reviewReview of recent literature pertaining to frequency, associations, mechanisms, and overall significance of sleep-wake disturbances (SWD) in the premotor and early phase of Parkinson's disease.Recent findings SWD are frequent in Parkinson's disease and their prevalence increases with disease progression. Recent studies confirm previous findings that SWD can appear as initial manifestation of Parkinson's disease even decades before motor signs appear and highlight their clinical associations in these early stages. More intriguingly, new evidence underpins their role as risk factors, predictors, or even as driving force for the neurodegenerative process. As our understanding of sleep-wake neurobiology increases, new hypotheses emerge concerning the pathophysiology of SWD in early Parkinson's disease stages involving dopaminergic and nondopaminergic mechanisms. INTRODUCTIONSleep-wake disturbances (SWD) are frequent in Parkinson's disease and are typically attributed to Parkinson's disease medications, poor sleep hygiene, and other nonmotor symptoms (NMS) such as nocturnal akinesia, pain, cramping, and nycturia. Over the past decade, notable advances have been made in the understanding of the role of the dopaminergic system in circadian mechanisms and sleep-wake physiology [1]. In addition, nondopaminergic systems are involved early in the pathogenesis of SWD in Parkinson's disease [2,3]. These findings suggest that SWD are no longer solely a complication of advanced PD but can emerge, among other NMS, in the premotor stages as a primary manifestation of neurodegeneration [4] and increase in frequency with Parkinson's disease progression (Fig. 1). Considering the importance of early diagnosis and intervention, the possibility that SWD may have prognostic value for the development of Parkinson's disease is intriguing.This review will discuss first the most recent literature on SWD in the context of premotor and early stage of Parkinson's disease and then important recent evidence on the pathophysiology of SWD in early Parkinson's disease. SUBJECTIVE SLEEP DISTURBANCES/ INSOMNIATwo thirds of patients with Parkinson's disease report poor sleep quality [5], many of them very early in the course of the disease [6,7]. Recent studies confirm the high prevalence of subjective sleep disturbances in the early stages of Parkinson's disease and highlight their association with low quality of life [8,9&& ,10 && ] and other NMS such as global cognitive impairment, anxiety, depression and nocturia [8]. Individuals later diagnosed with

show abstract

Section: Sleep-wake Neurobiology In Prodromal Parkinson's Diseasementioning

confidence: 99%

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

Bargiotas

Schuepbach

Bassetti

2016

Current Opinion in Neurology

View full text Add to dashboard Cite

show abstract

“…Samples were obtained from six young adult macaques, four of which had been treated weekly with low intravenous doses of MPTP (0.3 mg/kg) until stable Parkinsonism was established (Herrero et al 1993;Barcia et al 2003). This varied, depending on individual susceptibility to the toxin.…”

Section: Macaquesmentioning

confidence: 99%

Metalloproteinase-9 contributes to inflammatory glia activation and nigro-striatal pathway degeneration in both mouse and monkey models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism

et al. 2014

Self Cite

View full text Add to dashboard Cite

Inflammation is a predominant aspect of neurodegenerative diseases, manifested by glia activation and expression of pro-inflammatory mediators. Studies on animal models of Parkinson's disease (PD) suggest that sustained neuroinflammation exacerbates degeneration of the dopaminergic (DA) nigro-striatal pathway. Therefore, insights into the inflammatory mechanisms of PD may help the development of novel therapeutic strategies against this disease. As extracellular matrix metalloproteinases (MMPs) could be major players in the progression of Parkinsonism, we investigated, in the substantia nigra and striatum of mice acutely injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), changes in mRNA expression, protein levels, and cell localization of MMP-9. This protease is mainly neuronal, but early after MPTP injection its mRNA and protein levels, as well as the number of MMP-9-expressing microglia and astrocytes, increase concomitantly to a prominent inflammation. Neuroinflammation and MMP-9+ glia begin to decline within 2 weeks, although protein levels remain higher than control, in association with a partial recovery of DA nigro-striatal circuit. Comparable quantitative studies on MMP-9 knock-out mice, show a significant decrease in both glia activation and loss of DA neurons and fibers, with respect to wild-type. Moreover, in a parallel study on chronically MPTP-injected macaques, we observed that perpetuation of inflammation and high levels of MMP-9 are associated to DA neuron loss. Our data suggest that MMP-9 released by injured neurons favors glia activation; glial cells in turn reinforce their reactive state via autocrine MMP-9 release, contributing to nigro-striatal pathway degeneration. Specific modulation of MMP-9 activity may, therefore, be a strategy to ameliorate harmful inflammatory outcomes in Parkinsonism. © 2014 Springer-Verlag Berlin Heidelberg

show abstract

“…Four animals were treated with MPTP and four animals were untreated controls (Table 1). The monkeys were treated weekly with low doses of intravenous MPTP (0.3 mg/kg) according to previous protocols (Herrero et al, 1993;Barcia et al, 2003). Each animal received a different number of doses according to the level of Parkinsonism and their susceptibility to MPTP.…”

Section: Parkinsonian Monkeysmentioning

confidence: 99%