The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U
Open accessAbstract
TDP-43 is a multifunctional DNA/RNA-binding factor that has been implicated in the regulation of neuronal plasticity. TDP-43 has also been identified as the major constituent of the neuronal cytoplasmic inclusions (NCIs) that are characteristic of a range of neurodegenerative diseases, including the frontotemporal lobar degeneration with ubiquitin+ inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). We have generated a FTLD-U mouse model (CaMKII-TDP-43 Tg) in which TDP-43 is transgenically overexpressed in the forebrain resulting in phenotypic characteristics mimicking those of FTLD-U. In particular, the transgenic (Tg) mice exhibit impaired learning/memory, progressive motor dysfunction, and hippocampal atrophy. The cognitive and motor impairments are accompanied by reduced levels of the neuronal regulators phospho–extracellular signal-regulated kinase and phosphorylated cAMP response element-binding protein and increased levels of gliosis in the brains of the Tg mice. Moreover, cells with TDP-43+, ubiquitin+ NCIs and TDP-43–deleted nuclei appear in the Tg mouse brains in an age-dependent manner. Our data provide direct evidence that increased levels of TDP-43 protein in the forebrain is sufficient to lead to the formation of TDP-43+, ubiquitin+ NCIs and neurodegeneration. This FTLD-U mouse model should be valuable for the mechanistic analysis of the role of TDP-43 in the pathogenesis of FTLD-U and for the design of effective therapeutic approaches of the disease.
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Cites
Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis
Neumann, M., Sampathu, D. M., Kwong, L. K., Truax, A. C., Micsenyi, M. C., Chou, T. T., Bruce, J., Schuck, T., Grossman, M., Clark, C. M., et al. (2006) · Science · doi:10.1126/science.1134108 · Cited by 6,576
Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
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Control of memory formation through regulated expression of a CaMKII transgene
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Clinicopathological correlates in frontotemporal dementia
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Chen-Plotkin, A. S., Geser, F., Plotkin, J. B., Clark, C. M., Kwong, L. K., Yuan, W., Grossman, M., Van Deerlin, V. M., Trojanowski, J. Q., & Lee, V. M.-Y. (2008) · Human Molecular Genetics · doi:10.1093/hmg/ddn023 · Cited by 135 · cited 2×
“A global gene expression study has also found higher level of TDP-43 mRNA in several cases of PGRN mutation–positive FTLD-U (Chen-Plotkin et al., 2008).”
BackgroundMoisse, K., Mepham, J., Volkening, K., Welch, I., Hill, T., & Strong, M. J. (2009) · Brain Research · doi:10.1016/j.brainres.2009.07.023 · Cited by 93
Cited by
Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration
Lee, E. B., Lee, V. M.-Y., & Trojanowski, J. Q. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3121 · Cited by 659
Protein aggregation in amyotrophic lateral sclerosis
Blokhuis, A. M., Groen, E. J. N., Koppers, M., van den Berg, L. H., & Pasterkamp, R. J. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1125-6 · Cited by 579
Wang, I.-F., Guo, B.-S., Liu, Y.-C., Wu, C.-C., Yang, C.-H., Tsai, K.-J., & Shen, C.-K. J. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1206362109 · Cited by 377
Self-citationUnderstanding the role of TDP-43 and FUS/TLS in ALS and beyond
Da Cruz, S., & Cleveland, D. W. (2011) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2011.05.029 · Cited by 351
TDP-43 is intercellularly transmitted across axon terminals
Feiler, M. S., Strobel, B., Freischmidt, A., Helferich, A. M., Kappel, J., Brewer, B. M., Li, D., Thal, D. R., Walther, P., Ludolph, A. C., et al. (2015) · Journal of Cell Biology · doi:10.1083/jcb.201504057 · Cited by 329
Metadata
- Authors
- Tsai, K.-J., Yang, C.-H., Fang, Y.-H., Cho, K.-H., Chien, W.-L., Wang, W.-T., Wu, T.-W., Lin, C.-P., Fu, W.-M., & Shen, C.-K. J.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2010-07-26
- Volume
- 207
- Issue
- 8
- Pages
- 1661-1673
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2112343021
- Cited by
- 226
- References
- 7
- FWCI
- 11.29
- Type
- journal article
- Language
- en
- Open access
- green
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- The paper
- Tsai, K.-J., Yang, C.-H., Fang, Y.-H., Cho, K.-H., Chien, W.-L., Wang, W.-T., Wu, T.-W., Lin, C.-P., Fu, W.-M., & Shen, C.-K. J. (2010). Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20092164
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