TY - JOUR
T1 - Parkinson’s disease recovery by GM1 oligosaccharide treatment in the B4galnt1 +/− mouse model
AU - Chiricozzi, Elena
AU - Mauri, Laura
AU - Lunghi, Giulia
AU - Di Biase, Erika
AU - Fazzari, Maria
AU - Maggioni, Margherita
AU - Valsecchi, Manuela
AU - Prioni, Simona
AU - Loberto, Nicoletta
AU - Pomè, Diego Yuri
AU - Ciampa, Maria Grazia
AU - Fato, Pamela
AU - Verlengia, Gianluca
AU - Cattaneo, Stefano
AU - Assini, Robert
AU - Wu, Gusheng
AU - Alselehdar, Samar
AU - Ledeen, Robert W.
AU - Sonnino, Sandro
PY - 2019/12/1
Y1 - 2019/12/1
N2 - 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.
AB - 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.
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U2 - 10.1038/s41598-019-55885-2
DO - 10.1038/s41598-019-55885-2
M3 - Article
C2 - 31852959
AN - SCOPUS:85076886535
SN - 2045-2322
VL - 9
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 19330
ER -