{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T18:08:38Z","timestamp":1791828518845,"version":"4.3.4"},"reference-count":76,"publisher":"Wiley","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2014]]},"abstract":"<jats:p>Inflammation has been advocated as a possible common central mechanism for developmental cognitive impairment. Rett syndrome (RTT) is a devastating neurodevelopmental disorder, mainly caused by<jats:italic>de novo<\/jats:italic>loss-of-function mutations in the gene encoding MeCP2. Here, we investigated plasma acute phase response (APR) in stage II (i.e., \u201cpseudo-autistic\u201d) RTT patients by routine haematology\/clinical chemistry and proteomic 2-DE\/MALDI-TOF analyses as a function of four major<jats:italic>MECP2<\/jats:italic>gene mutation types (R306C, T158M, R168X, and large deletions). Elevated erythrocyte sedimentation rate values (median 33.0\u2009mm\/h versus 8.0\u2009mm\/h,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn fontstyle=\"italic\">0.0001<\/mml:mn><\/mml:math>) were detectable in RTT, whereas C-reactive protein levels were unchanged (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">0.63<\/mml:mn><\/mml:math>). The 2-DE analysis identified significant changes for a total of 17 proteins, the majority of which were categorized as APR proteins, either positive (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">6<\/mml:mn><\/mml:math>spots) or negative (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">9<\/mml:mn><\/mml:math>spots), and to a lesser extent as proteins involved in the immune system (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">2<\/mml:mn><\/mml:math>spots), with some proteins having overlapping functions on metabolism (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">7<\/mml:mn><\/mml:math>spots). The number of protein changes was proportional to the severity of the mutation. Our findings reveal for the first time the presence of a subclinical chronic inflammatory status related to the \u201cpseudo-autistic\u201d phase of RTT, which is related to the severity carried by the<jats:italic>MECP2<\/jats:italic>gene mutation.<\/jats:p>","DOI":"10.1155\/2014\/480980","type":"journal-article","created":{"date-parts":[[2014,1,9]],"date-time":"2014-01-09T05:51:36Z","timestamp":1389246696000},"page":"1-13","source":"Crossref","is-referenced-by-count":68,"title":["Subclinical Inflammatory Status in Rett Syndrome"],"prefix":"10.1155","volume":"2014","author":[{"given":"Alessio","family":"Cortelazzo","sequence":"first","affiliation":[{"name":"Child Neuropsychiatry Unit, University Hospital Azienda Ospedaliera Universitaria Senese (AOUS), Viale M. Bracci 16, 53100 Siena, Italy"},{"name":"Department of Medical Biotechnologies, University of Siena, Via A. Moro 2, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudio","family":"De Felice","sequence":"additional","affiliation":[{"name":"Neonatal Intensive Care Unit, University Hospital AOUS, Viale M. Bracci 16, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberto","family":"Guerranti","sequence":"additional","affiliation":[{"name":"Department of Medical Biotechnologies, University of Siena, Via A. Moro 2, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0006-9414","authenticated-orcid":true,"given":"Cinzia","family":"Signorini","sequence":"additional","affiliation":[{"name":"Department of Molecular and Developmental Medicine, University of Siena, Via A. Moro 6, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7027-1207","authenticated-orcid":true,"given":"Silvia","family":"Leoncini","sequence":"additional","affiliation":[{"name":"Child Neuropsychiatry Unit, University Hospital Azienda Ospedaliera Universitaria Senese (AOUS), Viale M. Bracci 16, 53100 Siena, Italy"},{"name":"Department of Molecular and Developmental Medicine, University of Siena, Via A. Moro 6, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5207-068X","authenticated-orcid":true,"given":"Alessandra","family":"Pecorelli","sequence":"additional","affiliation":[{"name":"Child Neuropsychiatry Unit, University Hospital Azienda Ospedaliera Universitaria Senese (AOUS), Viale M. Bracci 16, 53100 Siena, Italy"},{"name":"Department of Molecular and Developmental Medicine, University of Siena, Via A. Moro 6, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3350-4857","authenticated-orcid":true,"given":"Gloria","family":"Zollo","sequence":"additional","affiliation":[{"name":"Child Neuropsychiatry Unit, University Hospital Azienda Ospedaliera Universitaria Senese (AOUS), Viale M. Bracci 16, 53100 Siena, Italy"},{"name":"Department of Molecular and Developmental Medicine, University of Siena, Via A. Moro 6, 53100 Siena, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Landi","sequence":"additional","affiliation":[{"name":"Department of Life Science, University of Siena, Via A. 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