Clinicopathological feature of limbic-predominant age-related TDP-43 encephalopathy (LATE) in Lewy body disease and Alzheimer’s disease: Research Introduction
Author:
Affiliation:
1. Department of Neurology, Kyoto University Graduate School of Medicine
Publisher
The Society of Japanese Women Scientists
Subject
General Medicine
Link
https://www.jstage.jst.go.jp/article/sjws/24/0/24_240005/_pdf
Reference28 articles.
1. 1) Jo M, Lee S, Jeon YM, Kim S, et al. The role of TDP-43 propagation in neurodegenerative diseases: integrating insights from clinical and experimental studies. Exp Mol Med. 2020;52(10):1652-1662. doi:10.1038/s12276-020-00513-7
2. 2) Ratti A and Buratti E. Physiological functions and pathobiology of TDP‐43 and FUS/TLS proteins. J Neurochem. 2016;138:95-111. doi:10.1111/jnc.13625
3. 3) Neumann M, Sampathu DM, Kwong LK, et al. Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis. Science. 2006;314(5796):130-133. doi:10.1126/science.1134108
4. 4) Arai T, Hasegawa M, Akiyama H, et al. TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Biochem Bioph Res Co. 2006;351(3):602-611. doi:10.1016/j.bbrc.2006.10.093
5. 5) Nelson PT, Dickson DW, Trojanowski JQ, et al. Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report. Brain: a journal of neurology. Published online 2019. doi:10.1093/brain/awz099
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