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This is a personal, informal and non-sponsored commentary on papers recently published by the Italian biomedical research community.
The purpose is to draw attention not only to good Italian research,
but also to examples of good scientific reporting and publishing practices.
The selection of articles is purely subjective, but your suggestions are most welcome. Write to me, Valerie Matarese, Ph.D. at vmatarese @ uptoit.org (copies of non-OA papers are welcome).
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Up To it! Home > Italian biomedical research highlights > December 2008
Italian researchers have recently made valuable contributions to understanding the pathogenesis of two neurodegenerative diseases, Huntington's disease (HD) and multiple sclerosis (MS).
Researchers from Rome, with colleagues in Genoa and Fukuoka, examined the link between oxidative DNA damage and neurodegeneration. They asked if the oxidative DNA damage observed in brain of patients who died of HD was the cause—or an effect—of the neurodegenerative process. Their work focused on the protective role of hMTH1, one of several enzymes that hydrolyze oxidized nucleotides, preventing their incorporation into DNA. In this study, embryonic fibroblasts from transgenic mice overexpressing hMTH1 had significantly lower levels of 8-oxo-7,8-dihydroguanine (8-oxodG) in DNA than did cells from control mice, at baseline and after treatment with an oxidant. Moreover, when control and transgenic mice were treated with 3-nitroproprionic acid (a mitochondrial toxin that kills striatal neurons and induces symptomatology similar to HD), overexpression of hMTH1 conferred a significant protective effect, seen as fewer, smaller striatal lesions, less severe neurological manifestations and reduced mortality. Altogether, the study shows that clearance of oxidized dihydroguanine from the nucleotide pool reduces the amount of oxidized DNA and protects against chemically induced HD in mice. These results suggest a causal role for oxidized nucleic acids in the neuropathology of HD. The study was published in PLoS Genetics (PMID: 19023407).
The second paper, contributed by researchers from four northern Italian cities, used an immunomics approach to identify the targets of autoantibodies in patients with MS, an autoimmune disease involving demyelination and axonal degeneration. Serum and cerebrospinal fluid from 18 patients with MS and 20 controls were searched for IgG reactivity to normal human white matter proteins, by 2D immunoblotting; immunoreactive proteins were identified by mass spectrometry. The researchers identified 19 proteins selectively reactive with IgG from MS patients, including the oligodendral proteins transketolase and 2',3'-cyclic-nucleotide 3'-phosphodiesterase type I and several neuronal cytoskeletal proteins. These proteins merit further investigation for their role in the pathogenesis of MS and for their potential use as biomarkers for disease progression. The study was published in Molecular and Cellular Proteomics (PMID: 18676363). Posted 5 December 2008
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