Parkinson’s disease recovery by GM1 oligosaccharide treatment in the B4galnt1 +/− mouse model
| Autor: | Elena Chiricozzi, Margherita Maggioni, Maria Fazzari, Erika Di Biase, Pamela Fato, Gianluca Verlengia, Gusheng Wu, Diego Yuri Pomè, Simona Prioni, Giulia Lunghi, Laura Mauri, Stefano Cattaneo, Robert Assini, Sandro Sonnino, Robert W. Ledeen, Nicoletta Loberto, Samar K. Alselehdar, Manuela Valsecchi, Maria Grazia Ciampa |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Parkinson's disease Tyrosine 3-Monooxygenase Oligosaccharides lcsh:Medicine Pharmacology Motor Activity Article 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Neurotransmitter lcsh:Science chemistry.chemical_classification Neurotransmitter Agents Multidisciplinary Ganglioside biology Tyrosine hydroxylase Hand Strength Chemistry lcsh:R Parkinson Disease Oligosaccharide medicine.disease Phenotype nervous system diseases Mice Inbred C57BL Substantia Nigra Disease Models Animal 030104 developmental biology Membrane protein nervous system Preclinical research biology.protein alpha-Synuclein Diseases of the nervous system N-Acetylgalactosaminyltransferases Female lcsh:Q 030217 neurology & neurosurgery Neurotrophin |
| Zdroj: | Scientific Reports, Vol 9, Iss 1, Pp 1-15 (2019) Scientific Reports |
| ISSN: | 2045-2322 |
| Popis: | Given the recent in vitro discovery that the free soluble oligosaccharide of GM1 is the bioactive portion of GM1 for neurotrophic functions, we investigated its therapeutic potential in the B4galnt1+/− mice, a model of sporadic Parkinson’s disease. We found that the GM1 oligosaccharide, systemically administered, reaches the brain and completely rescues the physical symptoms, reduces the abnormal nigral α-synuclein content, restores nigral tyrosine hydroxylase expression and striatal neurotransmitter levels, overlapping the wild-type condition. Thus, this study supports the idea that the Parkinson’s phenotype expressed by the B4galnt1+/− mice is due to a reduced level of neuronal ganglioside content and lack of interactions between the oligosaccharide portion of GM1 with specific membrane proteins. It also points to the therapeutic potential of the GM1 oligosaccharide for treatment of sporadic Parkinson’s disease. |
| Databáze: | OpenAIRE |
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