http://www.cnr.it/ontology/cnr/individuo/prodotto/ID27065
F(4)-neuroprostanes mediate neurological severity in Rett syndrome. (Articolo in rivista)
- Type
- Label
- F(4)-neuroprostanes mediate neurological severity in Rett syndrome. (Articolo in rivista) (literal)
- Anno
- 2011-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.cca.2011.04.016 (literal)
- Alternative label
Signorini C, De Felice C, Leoncini S, Giardini A, D'Esposito M, Filosa S, Della Ragione F, Rossi M, Pecorelli A, Valacchi G, Ciccoli L, Hayek J. (2011)
F(4)-neuroprostanes mediate neurological severity in Rett syndrome.
in Clinica chimica acta (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Signorini C, De Felice C, Leoncini S, Giardini A, D'Esposito M, Filosa S, Della Ragione F, Rossi M, Pecorelli A, Valacchi G, Ciccoli L, Hayek J. (literal)
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- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- [ 1 ] AOUS, Univ Hosp, Neonatal Intens Care Unit, I-53100 Siena, Italy
[ 2 ] Univ Siena, Dept Pathophysiol Expt Med & Publ Hlth, I-53100 Siena, Italy
[ 3 ] CNR, Inst Genet & Biophys Adriano Buzzati Traverso, I-80125 Naples, Italy
[ 4 ] Ist Neurol Mediterraneo Neuromed, Pozzilli, Italy
[ 5 ] AOUS, Univ Hosp, Resp Pathophysiol & Rehabil Unit, I-53100 Siena, Italy
[ 6 ] Univ Siena, Dept Biomed Sci, I-53100 Siena, Italy
[ 7 ] Kyung Hee Univ, Dept Food & Nutr, Seoul, South Korea
[ 8 ] AOUS, Univ Hosp, Child Neuropsychiat Unit, I-53100 Siena, Italy (literal)
- Titolo
- F(4)-neuroprostanes mediate neurological severity in Rett syndrome. (literal)
- Abstract
- Rett syndrome (RTT) is a pervasive development disorder, mainly caused by mutations in the methyl-CpG binding protein 2 (MeCP2) gene. No reliable biochemical markers of the disease are available. Here we assess F(4)-neuroprostanes (F(4)-NeuroPs), lipid peroxidation products of the docosahexaenoic acid, as a novel disease marker in RTT and correlate it with clinical presentation, MeCP2 mutation type, and disease progression. In addition, we investigate on the impact of É-3 polyunsaturated fatty acids (É-3 PUFAs) supplementation on F(4)-NeuroPs levels.
METHODS:
A case-control study design was used. A cohort of RTT patients (n=144) exhibiting different clinical presentations, disease stages, and MeCP2 gene mutations were evaluated. F(4)-NeuroPs were measured in free form using a GC/NICI-MS/MS technique. Plasma F(4)-NeuroPs levels in patients were compared to healthy controls and related to RTT forms, disease progression, and response to É-3 PUFAs supplementation.
RESULTS:
Plasma F(4)-NeuroPs levels were i) higher in RTT than in controls; ii) increased with the severity of neurological symptoms; iii) significantly elevated during the typical disease progression; iv) higher in MeCP2-nonsense as compared to missense mutation carriers; v) higher in typical RTT as compared to RTT variants; and vi) decreased in response to 12months É-3 PUFAs oral supplementation.
CONCLUSIONS:
Quantification of plasma F(4)-NeuroPs provides a novel RTT marker, related to neurological symptoms severity, mutation type and clinical presentation. (literal)
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- Autore CNR
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