Carotid body autotransplantation in Parkinson disease: a clinical and positron emission tomography study

Minguez-Castellanos, Adolfo; Escamilla-Sevilla, Francisco; Hotton, Gary; Toledo‐Aral, Juan José; Ortega-Moreno, A; Méndez‐Ferrer, Simón; Martin-Linares, J. M.; Katati, Majed J.; Mir, Pablo; Villadiego, Javier; Meersmans, M.; Pérez-Garcı́a, Miguel; Brooks, David J.; Arjona, V.; López‐Barneo, José

doi:10.1136/jnnp.2006.106021

Cited by 94 publications

(65 citation statements)

References 41 publications

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“…The urinary excretion of the O-methylated metabolite of dopamine, 3-methoxytyramine, was increased in 10 out of the 28 patients, but could be present in a variety of patients with or without pheochromocytomas, extra-adrenal paragangliomas, malignant disease, and producing glomus tumors. Interestingly, the elevated levels of 3-methoxytyramine in our study could be a reflection of the fact that we used the presence of HNP as an inclusion criterion, because carotid bodies are known to use dopamine as a neurotransmitter (Koch et al 2003, Jeffery et al 2006, Minguez-Castellanos et al 2007). We suspect HNP might continuously O-methylate dopamine and subsequently release methoxytyramine into the circulation, even in the absence of overt dopamine secretion.…”

Section: B Havekes Et Al: Screening In Sdhd Patientsmentioning

confidence: 99%

Pheochromocytomas and extra-adrenal paragangliomas detected by screening in patients with SDHD-associated head-and-neck paragangliomas

Havekes

Klaauw²,

Weiss³

et al. 2009

Endocrine-Related Cancer

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Patients with SDHD-associated head-and-neck paragangliomas (HNP) are at risk for developing pheochromocytomas for which screening has been advised. To assess clinical, biochemical, and radiological outcomes of screening in a large single-center cohort of SDHD-positive patients with HNP and to address the necessity for repetitive follow-up, we evaluated 93 patients with SDHDassociated HNP (p.Asp92Tyr, p.Leu139Pro). Screening consisted of measurement of 24 h urinary excretion of catecholamines and/or their metabolites in duplicate, which was repeated with intervals of 2 years if initial biochemical screening was negative. In patients, in whom urinary excretion was above the reference limit, imaging studies with 123 I-MIBG (metaiodobenzylguanidine) scintigraphy and magnetic resonance imaging (MRI) and/or computed tomography (CT) were performed. Pheochromocytomas and extra-adrenal paragangliomas were treated surgically after appropriate blockade. Median follow-up was 4.5 years (range 0.5-19.5 years). Twenty-eight out of the 93 patients were included in our study and underwent additional imaging for pheochromocytomas/extra-adrenal paragangliomas. In 11 out of the 28 patients intra-adrenal pheochromocytomas were found. Extra-adrenal paragangliomas were discovered in eight patients. These tumors were detected during initial screening in 63% of cases, whereas 37% were detected after repeated biochemical screening. One patient was diagnosed with a biochemically silent pheochromocytoma. The high prevalence of pheochromocytomas/extra-adrenal paragangliomas in patients with SDHD-associated HNP warrants regular screening for tumors in these patients. Paragangliomas that do not secrete catecholamines might be more prevalent than previously reported. Future studies will have to establish whether routine imaging studies should be included in the screening of SDHD mutation carriers, irrespective of biochemical screening.

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Section: B Havekes Et Al: Screening In Sdhd Patientsmentioning

confidence: 99%

Pheochromocytomas and extra-adrenal paragangliomas detected by screening in patients with SDHD-associated head-and-neck paragangliomas

Havekes

Klaauw²,

Weiss³

et al. 2009

Endocrine-Related Cancer

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“…Some groups have assayed the effect of intrastriatal transplantation of GDNF-producing cells, such as those in the carotid body, with moderate results (Arjona et al 2003). Currently, in vitro carotid body expansion is being tested using animal (Pardal et al 2007) and human tissue to increase the number of cells available for transplantation (see Minguez-Castellanos et al 2007). In parallel with these 'cell therapy' studies, several clinical trials have been performed using the direct intracerebral infusion of GDNF.…”

Section: Clinical Effects Of Gdnfmentioning

confidence: 99%

GDNF and protection of adult central catecholaminergic neurons

Pascual

Hidalgo-Figueroa²,

Gómez-Díaz³

et al. 2011

Journal of Molecular Endocrinology

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Neurotrophic factors are small proteins necessary for neuron survival and maintenance of phenotype. They are considered as promising therapeutic tools for neurodegenerative diseases. The glial cell line-derived neurotrophic factor (GDNF) protects catecholaminergic cells from toxic insults; thus, its potential therapeutic applicability in Parkinson's disease has been intensely investigated. In recent years, there have been major advances in the analysis of GDNF signaling pathways in peripheral neurons and embryonic dopamine mesencephalic cells. However, the actual physiological role of GDNF in maintaining catecholaminergic central neurons during adulthood is only starting to be unraveled, and the mechanisms whereby GDNF protects central brain neurons are poorly known. In this study, we review the current knowledge of GDNF expression, signaling, and function in adult brain, with special emphasis on the genetic animal models with deficiency in the GDNF-dependent pathways.

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“…In fact, carotid body grafting has also been shown to reduce neuronal death in an acute rat stroke model [105]. The systematic clinical applicability of carotid body dopamine-and glia cell line-derived neurotrophic factor-producing cells is under investigation [1,106].…”

Section: Carotid Body and Cell Therapymentioning

confidence: 99%

Carotid body oxygen sensing

López‐Barneo¹,

Ortega-Sáenz²,

Pardal³

et al. 2008

European Respiratory Journal

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122

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The carotid body (CB) is a neural crest-derived organ whose major function is to sense changes in arterial oxygen tension to elicit hyperventilation in hypoxia. The CB is composed of clusters of neuron-like glomus, or type-I, cells enveloped by glia-like sustentacular, or type-II, cells. Responsiveness of CB to acute hypoxia relies on the inhibition of O 2 -sensitive K + channels in glomus cells, which leads to cell depolarisation, Ca 2+ entry and release of transmitters that activate afferent nerve fibres. Although this model of O 2 sensing is generally accepted, the molecular mechanisms underlying K + channel modulation by O 2 tension are unknown. Among the putative hypoxia-sensing mechanisms there are: the production of oxygen radicals, either in mitochondria or reduced nicotinamide adenine dinucleotide phosphate oxidases; metabolic mitochondrial inhibition and decrease of intracellular ATP; disruption of the prolylhydroxylase/ hypoxia inducible factor pathway; or decrease of carbon monoxide production by haemoxygenase-2. In chronic hypoxia, the CB grows with increasing glomus cell number. The current authors have identified, in the CB, neural stem cells, which can differentiate into glomus cells. Cell fate experiments suggest that the CB progenitors are the glia-like sustentacular cells. The CB appears to be involved in the pathophysiology of several prevalent human diseases.

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Carotid body autotransplantation in Parkinson disease: a clinical and positron emission tomography study

Cited by 94 publications

References 41 publications

Pheochromocytomas and extra-adrenal paragangliomas detected by screening in patients with SDHD-associated head-and-neck paragangliomas

Pheochromocytomas and extra-adrenal paragangliomas detected by screening in patients with SDHD-associated head-and-neck paragangliomas

GDNF and protection of adult central catecholaminergic neurons

Carotid body oxygen sensing

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