The DOI matches its Crossref record; 132 of the 132 references it cites were found in a registry or an index.
Synaptic dysfunction in Huntington's disease: a new perspective
Open accessAbstract
Huntington's disease (HD) is caused by a polyglutamine expansion in the protein huntingtin and is characterized by intraneuronal inclusions and widespread neuronal death at the late stage of the disease. In research, most of the emphasis has been on understanding the cell death and its mechanisms. Until recently, it was believed that the vast majority, if not all, of the symptoms in HD are a direct consequence of neurodegeneration. However, increasing evidence shows that subtle alterations in synaptic function could underlie the early symptoms. It is of particular interest to understand the nature of this neuronal dysfunction. Normal huntingtin interacts with various cytoskeletal and synaptic vesicle proteins that are essential for exocytosis and endocytosis. Altered interactions of mutant huntingtin with its associated partners could contribute to abnormal synaptic transmission in HD. This review describes recent advances in understanding synaptic dysfunction in HD.
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In the citing paper
“Studies suggest that wild-type huntingtin has a role in vesicular trafficking and axonal transport (Gauthier et al., 2004;Trushina et al., 2004;Smith et al., 2005a;Caviston and Holzbaur, 2009).”
From Dendritic Spine Instability Leads to Progressive Neocortical Spine Loss in a Mouse Model of Huntington's Disease (2013) · cites this paper as Smith et al., 2005a
In the citing paper
“These aggregates could impair synaptic function, distort dendritic morphology, and disrupt trafficking and cell signaling and contribute to the known dendritic pathology that occurs in HD (Li et al., 2003;Smith et al., 2005a).”
From Dendritic Spine Instability Leads to Progressive Neocortical Spine Loss in a Mouse Model of Huntington's Disease (2013) · cites this paper as Smith et al., 2005a
Citations
Cites
Molecular Chaperones in the Cytosol: from Nascent Chain to Folded Protein
Hartl, F. U., & Hayer-Hartl, M. K. (2002) · Science · doi:10.1126/science.1068408 · Cited by 3,335
Mangiarini, L., Sathasivam, K., Seller, M., Cozens, B., Harper, A., Hetherington, C., Lawton, M., Trottier, Y., Lehrach, H., Davies, S. W., et al. (1996) · Cell · doi:10.1016/s0092-8674(00)81369-0 · Cited by 3,073
Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in Brain
DiFiglia, M., Sapp, E., Chase, K. O., Davies, S. W., Bates, G. P., Vonsattel, J. P., & Aronin, N. (1997) · Science · doi:10.1126/science.277.5334.1990 · Cited by 2,439
Neuropathological Classification of Huntingtonʼs Disease
VONSATTEL, J.-P., MYERS, R. H., STEVENS, T. J., FERRANTE, R. J., BIRD, E. D., & RICHARDSON, E. P. (1985) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-198511000-00003 · Cited by 2,227
Saudou, F., Finkbeiner, S. M., Devys, D., & Greenberg, M. E. (1998) · Cell · doi:10.1016/s0092-8674(00)81782-1 · Cited by 1,598
Synaptic Vesicle Phosphoproteins and Regulation of Synaptic Function
Greengard, P., Valtorta, F., Czernik, A. J., & Benfenati, F. (1993) · Science · doi:10.1126/science.8430330 · Cited by 1,311
Gauthier, L. R., Charrin, B. C., Borrell-Pagès, M., Dompierre, J. P., Rangone, H., Cordelières, F. P., De Mey, J., MacDonald, M. E., Leßmann, V., Humbert, S., et al. (2004) · Cell · doi:10.1016/j.cell.2004.06.018 · Cited by 1,178
Nucifora, F. C., Sasaki, M., Peters, M. F., Huang, H., Cooper, J. K., Yamada, M., Takahashi, H., Tsuji, S., Troncoso, J. C., Dawson, V. L., et al. (2001) · Science · doi:10.1126/science.1056784 · Cited by 1,112
Steffan, J. S., Kazantsev, A. G., Spasić-Bošković, O., Greenwald, M., Zhu, Y., Goehler, H., Wanker, E. E., Bates, G. P., Housman, D. E., & Thompson, L. M. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.100110097 · Cited by 1,057
Chaperone-Mediated Protein Folding
Fink, A. L. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.2.425 · Cited by 1,055
Cited by
Sorted by citations
Molecular Mechanisms and Potential Therapeutical Targets in Huntington's Disease
Zuccato, C., Valenza, M., & Cattaneo, E. (2010) · Physiological Reviews · doi:10.1152/physrev.00041.2009 · Cited by 848
Normal huntingtin function: an alternative approach to Huntington's disease
Cattaneo, E. F., Zuccato, C., & Tartari, M. (2005) · Nature reviews. Neuroscience · doi:10.1038/nrn1806 · Cited by 655
Sheldon, A. L., & Robinson, M. B. (2007) · Neurochemistry International · doi:10.1016/j.neuint.2007.03.012 · Cited by 593
Localization of LRRK2 to membranous and vesicular structures in mammalian brain
Biskup, S., Moore, D. J., Celsi, F., Higashi, S., West, A. B., Andrabi, S. A., Kurkinen, K. M. A., Yu, S., Savitt, J. M., Waldvogel, H. J., et al. (2006) · Annals of Neurology · doi:10.1002/ana.21019 · Cited by 530
Mechanisms of neurodegeneration in Huntington’s disease
Gil‐Mohapel, J., & Rego, A. C. (2008) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2008.06310.x · Cited by 497
Metadata
- Authors
- Smith, R., Brundin, P., & Li, J.-Y.
- Affiliations
- Lund University (SE)
- Corresponding author
- Li, J.-Y.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2005-06-15
- Volume
- 62
- Issue
- 17
- Pages
- 1901-1912
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11139070
- OpenAlex
- W2132164151
- Cited by
- 166
- References
- 132
- Citations by year
- 2026: 2 · 2025: 3 · 2023: 4 · 2022: 5 · 2021: 7 · 2020: 8 · 2019: 4 · 2018: 10 · 2017: 8 · 2016: 10 · 2015: 4 · 2014: 10 · 2013: 10 · 2012: 12
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- Huntington's disease, synaptic dysfunction, huntingtin, polyglutamine expansion, mutant huntingtin, synaptic vesicle proteins, exocytosis, endocytosis, synaptic transmission, neurodegeneration, neuronal dysfunction
- MeSH terms
- Huntingtin Protein, Animals, Brain, Exocytosis, Humans, Huntington Disease, Mutation, Nerve Tissue Proteins, Synaptic Transmission, Nuclear Proteins, Synapses, Transcription, Genetic, Models, Animal
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