Impaired levels of gangliosides in the corpus callosum of Huntington disease animal models

Frontiers in Neuroscience

Volumn 10, Issue OCT, 2016, Pages

  Di Pardo, Alba Di ^a   Amico, Enrico ^a   Maglione, Vittorio ^a  

^a IRCCS NEUROMED   (Italy)

Author keywords

Corpus callosum white matter (CC WM); Gangliosides; GD1a; GM1; GT1b; HD

Indexed keywords

GANGLIOSIDE GD 1A; GANGLIOSIDE GM1; GANGLIOSIDE GT 1B; GLYCOSPHINGOLIPID;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN CORTEX; BRAIN TISSUE; CONTROLLED STUDY; CORPUS CALLOSUM; CORPUS STRIATUM; HUNTINGTON CHOREA; MOUSE; NONHUMAN; PATHOGENESIS; TRANSGENIC MOUSE; WHITE MATTER;

EID: 84997079101     PISSN: 16624548     EISSN: 1662453X     Source Type: Journal    
DOI: 10.3389/fnins.2016.00457     Document Type: Article

References (31)

1. Bohanna, I., Georgiou-Karistianis, N., Sritharan, A., Asadi, H., Johnston, L., Churchyard, A., et al. (2011). Diffusion tensor imaging in Huntington's disease reveals distinct patterns of white matter degeneration associated with motor and cognitive deficits. Brain Imaging Behav. 5, 171-180. doi: 10.1007/s11682-011-9121-8.
2. Bradford, J., Shin, J. Y., Roberts, M., Wang, C. E., Li, X. J., and Li, S. (2009). Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms. Proc. Natl. Acad. Sci. U.S.A. 106, 22480-22485. doi: 10.1093/cercor/bhr360.
3. Bradford, J., Shin, J. Y., Roberts, M., Wang, C. E., Shang, G., Li, S., et al. (2010). Mutant huntingtin in glial cells exacerbates neurological symptoms of Huntington disease mice. J. Biol. Chem. 285, 10653-10661. doi: 10.1074/jbc.M109.083287.
4. Ciarmiello, A., Cannella, M., Lastoria, S., Simonelli, M., Frati, L., Rubinsztein, D. C., et al. (2006). Brain white-matter volume loss and glucose hypometabolism precede the clinical symptoms of Huntington's disease. J. Nucl. Med. 47, 215-222.
5. Denny, C. A., Desplats, P. A., Thomas, E. A., and Siegfried, T. N. (2010). Cerebellar lipid differences between R6/1 transgenic mice and humans with Huntington's disease. J. Neurochem. 115, 748-758. doi: 10.1111/j.1471-4159.2010.06964.x.
6. Desplats, P. A., Denny, C. A., Kass, K. E., Gilmartin, T., Head, S. R., Sutcliffe, J. G., et al. (2007). Glycolipid and ganglioside metabolism imbalances in Huntington's disease. Neurobiol. Dis. 27, 265-277. doi: 10.1016/j.nbd.2007.05.003.
7. Di Paola, M., Luders, E., Cherubini, A., Sanchez-Castaneda, C., Thompson, P. M., Toga, A. W., et al. (2012). Multimodal MRI analysis of the corpus callosum reveals white matter differences in presymptomatic and early Huntington's disease. Cereb. Cortex 22, 2858-2866. doi: 10.1093/cercor/bhr360.
8. Di Paola, M., Phillips, O. R., Sanchez-Castaneda, C., Di Pardo, A., Maglione, V., Caltagirone, C., et al. (2014). MRI measures of corpus callosum iron and myelin in early Huntington's disease. Hum. Brain Mapp. 35, 3143-3151. doi: 10.1002/hbm.22391.
9. Di Pardo, A., Amico, E., Favellato, M., Castrataro, R., Fucile, S., Squitieri, F., et al. (2014). FTY720 (fingolimod) is a neuroprotective and disease-modifying agent in cellular and mouse models of Huntington disease. Hum. Mol. Genet. 23, 2251-2265. doi: 10.1093/hmg/ddt615.
10. Dumas, E. M., van den Bogaard, S. J., Hart, E. P., Soeter, R. P., van Buchem, M. A., van der Grond, J., et al. (2013). TRACK-H, investigator group. Reduced functional brain connectivity prior to and after disease onset in Huntington's disease. Neuroimage Clin. 2, 377-384. doi: 10.1016/j.nicl.2013.03.001.
11. Fennema-Notestine, C., Archibald, S. L., Jacobson, M. W., Corey-Bloom, J., Paulsen, J. S., Peavy, G. M., et al. (2004). In vivo evidence of cerebellar atrophy and cerebral white matter loss in Huntington disease. Neurology 63, 989-995. doi: 10.1212/01.WNL.0000138434.68093.67.
12. Gatto, R. G., Chu, Y., Ye, A. Q., Price, S. D., Tavassoli, E., Buenaventura, A., et al. (2015). Analysis of YFP(J16)-R6/2 reporter mice and postmortem brains reveal early pathology and increased vulnerability of callosal axons in Huntington's disease. Hum. Mol. Genet. 24, 5285-5298. doi: 10.1093/hmg/ddv248.
13. Han, I., You, Y., Kordower, J. H., Brady, S. T., and Morfini, G. A. (2010). Differential vulnerability of neurons in Huntington's disease: the role of cell type-specific features. J. Neurochem. 113, 1073-1091. doi: 10.1111/j.1471-4159.2010.06672.x.
14. Hsiao, H. Y., and Chern, Y. (2010). Targeting glial cells to elucidate the pathogenesis of Huntington's disease. Mol. Neurobiol. 41, 248-255. doi: 10.1007/s12035-009-8097-5.
15. Huang, B., Wei, W., Wang, G., Gaertig, M. A., Feng, Y., Wang, W., et al. (2015). Mutant huntingtin downregulates myelin regulatory factor-mediated myelin gene expression and affects mature oligodendrocytes. Neuron 85, 1212-1226. doi: 10.1016/j.neuron.2015.02.026.
16. Jin, J., Peng, Q., Hou, Z., Jiang, M., Wang, X., Langseth, A. J., et al. (2015). Early white matter abnormalities, progressive brain pathology and motor deficits in a novel knock-in mouse model of Huntington's disease. Hum. Mol. Genet. 24, 2508-2527. doi: 10.1093/hmg/ddv016.
17. Kim, S. U. (1990). Neurobiology of human oligodendrocytes in culture. J. Neurosci. Res. 27, 712-728.
18. Lerch, J. P., Carroll, J. B., Dorr, A., Spring, S., Evans, A. C., Hayden, M. R., et al. (2008). Cortical thickness measured from MRI in the YAC128 mouse model of Huntington's disease. Neuroimage 41, 243-251. doi: 10.1016/j.neuroimage.2008.02.019.
19. Li, H., Li, S. H., Yu, Z. X., Shelbourne, P., and Li, X. J. (2001). Huntingtin aggregate-associated axonal degeneration is an early pathological event in Huntington's disease mice. J. Neurosci. 21, 8473-8481.
20. Maglione, V., Marchi, P., Di Pardo, A., Lingrell, S., Horkey, M., Tidmarsh, E., et al. (2010). Impaired ganglioside metabolism in Huntington's disease and neuroprotective role of GM1. J. Neurosci. 30, 4072-4080. doi: 10.1523/JNEUROSCI.6348-09.2010.
21. Novak, M. J., and Tabrizi, S. J. (2011). Huntington's disease: clinical presentation and treatment. Int. Rev. Neurobiol. 98, 297-323. doi: 10.1016/B978-0-12-381328-2.00013-4.
22. Posse de Chaves, E., and Sipione, S. (2010). Sphingolipids and gangliosides of the nervous system in membrane function and dysfunction. FEBS Lett. 589, 1748-1759. doi: 10.1016/j.febslet.2009.12.010.
23. Poudel, G. R., Stout, J. C., Domínguez, D. J. F., Salmon, L., Churchyard, A., Chua, P., et al. (2014). White matter connectivity reflects clinical and cognitive status in Huntington's disease. Neurobiol. Dis. 65, 180-187. doi: 10.1016/j.nbd.2014.01.013.
24. Rosas, H. D., Lee, S. Y., Bender, A. C., Zaleta, A. K., Vangel, M., Yu, P., et al. (2010). Altered white matter microstructure in the corpus callosum in Huntington's disease: implications for cortical "disconnection." Neuroimage 49, 2995-3004. doi: 10.1016/j.neuroimage.2009.10.015.
25. Sabourdy, F., Kedjouar, B., Sorli, S. C., Colié, S., Milhas, D., Salma, Y., et al. (2008). Functions of sphingolipid metabolism in mammals-lessons from genetic defects. Biochim. Biophys. Acta 1781, 145-183. doi: 10.1016/j.bbalip.2008.01.004.
26. Schnaar, R. L. (2010). Brain gangliosides in axon-myelin stability and axon regeneration. FEBS Lett. 584, 1741-1747. doi: 10.1016/j.febslet.2009.10.011.
27. Sheikh, K. A., Sun, J., Liu, Y., Kawai, H., Crawford, T. O., Proia, R. L., et al. (1999). Mice lacking complex gangliosides develop Wallerian degeneration and myelination defects. Proc. Natl. Acad. Sci. U.S.A. 96, 7532-7537.
28. Southwell, A. L., Franciosi, S., Villanueva, E. B., Xie, Y., Winter, L. A., Veeraraghavan, J., et al. (2015). Anti-semaphorin 4D immunotherapy ameliorates neuropathology and some cognitive impairment in the YAC128 mouse model of Huntington disease. Neurobiol. Dis. 76, 46-56. doi: 10.1016/j.nbd.2015.01.002.
29. The Huntington's Disease Collaborative Research Group (1993). A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. Cell 72, 971-983.
30. Xiang, Z., Valenza, M., Cui, L., Leoni, V., Jeong, H. K., Brilli, E., et al. (2011). Peroxisome-proliferator-activated receptor gamma coactivator 1 a contributes to dysmyelination in experimental models of Huntington's disease. J. Neurosci. 31, 9544-9553. doi: 10.1523/JNEUROSCI.1291-11.2011.
31. Yamashita, T., Wu, Y. P., Sandhoff, R., Werth, N., Mizukami, H., Ellis, J. M., et al. (2005). Interruption of ganglioside synthesis produces central nervous system degeneration and altered axon-glial interactions. Proc. Natl. Acad. Sci. U.S.A. 102, 2725-2730. doi: 10.1073/pnas.0407785102.