Title |
Changes of peripheral TGF-β1 depend on monocytes-derived macrophages in Huntington disease
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Published in |
Molecular Brain, December 2013
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DOI | 10.1186/1756-6606-6-55 |
Pubmed ID | |
Authors |
Alba Di Pardo, Silvia Alberti, Vittorio Maglione, Enrico Amico, Etty P Cortes, Francesca Elifani, Giuseppe Battaglia, Carla L Busceti, Ferdinando Nicoletti, JeanPaul G Vonsattel, Ferdinando Squitieri |
Abstract |
Huntington Disease (HD) is a neurodegenerative disorder resulting from the expansion of polyglutamine stretch in the huntingtin protein (Htt). Mutant HTT (mHtt) leads to progressive impairment of several molecular pathways that have been linked to disease pathogenesis. Defects in the production of a number of neurotrophic factors have been described as important determinants contributing to the development of HD. We have previously demonstrated that production of transforming growth factor-β1 (TGF-β1) is also deregulated in HD. Peripheral levels of TGF-β1 were markedly reduced early in the disease and returned to normal levels with disease severity. However, the cause and the biochemical origin of such abnormalities are still unclear. |
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Unknown | 1 | 100% |
Demographic breakdown
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Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
Geographical breakdown
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Italy | 1 | 2% |
Unknown | 47 | 96% |
Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 13 | 27% |
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Student > Bachelor | 3 | 6% |
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