Increased cerebrospinal fluid concentration of nitrite in Parkinsonʼs disease

Qureshi, G. Ali; Baig, Shahid; Bednar, I.; Södersten, P.; Forsberg, G.; Sidén, Å

doi:10.1097/00001756-199508000-00013

Cited by 126 publications

(80 citation statements)

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“…The hypothesis that raises NO/GC/cGMP pathway activity in the CNS is also supported by some evidence in Parkinsonian patients. Indeed, increased levels of NO second messenger cGMP in serum [194] and NO 3 in cerebrospinal fluid [195] have been detected in PD patients receiving L-DOPA therapy. Nevertheless, the precise role of NO in the pathogenesis of such invalidating complications remains elusive and recent mounting evidence seems to indicate an inhibition of cGMP levels rather than an increase after L-DOPA.…”

Section: Role Of No In L-dopa-induced Dyskinesiamentioning

confidence: 99%

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Pierucci

Galati

Valentino

et al. 2011

CNSNDDT

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Several recent studies have emphasized a crucial role for the nitrergic system in movement control and the pathophysiology of the basal ganglia (BG). These observations are supported by anatomical evidence demonstrating the presence of nitric oxide synthase (NOS) in all the basal ganglia nuclei. In fact, nitrergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high expression of nitric oxide (NO)-producing neurons, with the striatum having the greatest number, together with important NO afferent input. In this paper, the distribution of NO in the BG nuclei will be described. Furthermore, evidence demonstrating the nitrergic control of BG activity will be reviewed. The new avenues that the increasing knowledge of NO in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. For example, inhibition of striatal NO/guanosine monophosphate signal pathway by phosphodiesterases seems to be effective in levodopa-induced dyskinesia. However, the results of experimental studies have to be interpreted with caution given the complexities of nitrergic signalling and the limitations of animal models. Nevertheless, the NO system represents a promising pharmacological intervention for treating Parkinson's disease and related disorders.

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Section: Role Of No In L-dopa-induced Dyskinesiamentioning

confidence: 99%

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Pierucci

Galati

Valentino

et al. 2011

CNSNDDT

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“…Second, significant microglial activation occurs in close proximity to damaged or dying dopaminergic neurons. Third, the concentration of NO 2 Ϫ (nitrite), a metabolite of NO, increases in the cerebrospinal fluid (CSF) of patients with PD compared with patients without dopaminergic dysfunction (6). It has been shown that many cells in the SNpc from postmortem PD samples express considerable amounts of inducible nitric oxide synthase (iNOS), whereas those from age-matched controls do not (7).…”

mentioning

confidence: 99%

Selective inhibition of NF-κB activation prevents dopaminergic neuronal loss in a mouse model of Parkinson's disease

Ghosh

Roy

Liu

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

394

434

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Parkinson's disease (PD) is the second most common neurodegenerative disorder. Despite intense investigations, no effective therapy is available to stop its onset or halt its progression. The present study evaluates the ability of peptide corresponding to the NF-B essential modifier-binding domain (NBD) of I B kinase ␣ (IKK␣) or IKK␤ to prevent nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD and establish a role for NF-B in human parkinsonism. First, we found that NF-B was activated within the substantia nigra pars compacta of PD patients and MPTP-intoxicated mice. However, i.p. injection of wild-type NBD peptide reduced nigral activation of NF-B, suppressed nigral microglial activation, protected both the nigrostriatal axis and neurotransmitters, and improved motor functions in MPTP-intoxicated mice. These findings were specific because mutated NBD peptide had no effect. We conclude that selective inhibition of NF-B activation by NBD peptide may be of therapeutic benefit for PD patients.MPTP ͉ NBD peptides ͉ neurodegeneration

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“…Recent studies demonstrate that chronic inflammation in the central nervous system (CNS) is also a hallmark of various neurodegenerative disorders in which progressive loss of structure and function of neurons and neuronal death are observed (1)(2)(3)(4)(5). For example, the concentration of NO 2 Ϫ (nitrite), a metabolite of nitric oxide (NO), increases in the cerebrospinal fluid of patients with Parkinson disease and Alzheimer disease in comparison with agematched controls (6). Consistently, the ablation of inducible nitric-oxide synthase (iNOS) 2 in mutant mice significantly protects dopaminergic neurons from MPTP neurotoxicity, indicating that iNOS is essential in MPTP-induced substantia nigra pars compacta dopaminergic neurodegeneration (7).…”

mentioning

confidence: 99%

Suppression of Nuclear Factor-κB Activation and Inflammation in Microglia by Physically Modified Saline

Khasnavis

Jana

Roy

et al. 2012

Journal of Biological Chemistry

102

128

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Background: Microglial activation plays an important role in the pathogenesis of neurodegenerative disorders. Results: Taylor-Couette-Poiseuille flow-modified saline (RNS60) inhibits microglial inflammation via type 1A phosphatidylinositol 3-kinase-Akt-CREB-mediated up-regulation of IB␣ and inhibition of NF-B activation. Conclusion: These results delineate a novel biological function of a physically modified saline. Significance: RNS60 may be of therapeutic benefit in neurodegenerative disorders.

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Increased cerebrospinal fluid concentration of nitrite in Parkinsonʼs disease

Cited by 126 publications

References 0 publications

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Nitric Oxide Modulation of the Basal Ganglia Circuitry: Therapeutic Implication for Parkinson's Disease and Other Motor Disorders

Selective inhibition of NF-κB activation prevents dopaminergic neuronal loss in a mouse model of Parkinson's disease

Suppression of Nuclear Factor-κB Activation and Inflammation in Microglia by Physically Modified Saline

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