Cited by 66Alzheimer's disease research and treatmentsPrion Diseases and Protein MisfoldingAmyotrophic Lateral Sclerosis Research

The twenty-four KDa C-terminal tau fragment increases with aging in tauopathy mice: implications of prion-like properties

Matsumoto, Shin-Ei, Motoi, Yumiko, Ishiguro, Koichi, Tabira, Takeshi, Kametani, Fuyuki, Hasegawa, Masato, Hattori, Nobutaka·2015·Human Molecular Genetics

Abstract

The truncated tau protein is a component of the neurofibrillary tangles found in the brains with tauopathies. However, the molecular mechanisms by which the truncated tau fragment causes neurodegeneration remain unknown. Tau pathology was recently suggested to spread through intercellular propagation, and required the formation of 'prion-like' species. We herein identified a new fragment of the tau protein that consisted of four binding domains and a C-terminal tail (Tau-CTF24), but lacked the N-terminal projection domain, and found that it increased with aging in tauopathy model mice (Tg601). Tau-CTF24-like fragments were also present in human brains with tauopathies. A mass spectroscopic analysis revealed that Tau-CTF24 was cleaved behind R242. The digestion of full-length tau (Tau-FL) by calpain produced Tau-CTF24 in vitro and calpain activity increased in old Tg601. Recombinant Tau-CTF24 accelerated heparin-induced aggregation and lost the ability to promote microtubule assembly. When insoluble tau from diseased brains or aggregated recombinant tau was introduced as seeds into SH-SY5Y cells, a larger amount of insoluble tau was formed in cells overexpressing Tau-CTF24 than in those overexpressing Tau-FL. Furthermore, lysates containing the Tau-CTF24 inclusion propagated to naive tau-expressing cells more efficiently than those containing the Tau-FL inclusion. Immunoblot and confocal microscopic analyses revealed that aggregated Tau-CTF24 bound to cells more rapidly and abundantly than aggregated Tau-FL. Our results suggest that Tau-CTF24 contributes to neurodegeneration by enhancing prion-like propagation as well as deteriorating the mechanisms involved in microtubule function.

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Authors
Matsumoto, S.-E., Motoi, Y., Ishiguro, K., Tabira, T., Kametani, F., Hasegawa, M., & Hattori, N.
Affiliations
  • Juntendo University (JP)
  • Tokyo Metropolitan Institute of Medical Science (JP)
Corresponding author
Motoi, Yumiko
Venue
Human Molecular Genetics
Published
2015-09-15
Volume
24
Issue
22
Pages
6403-6416
ISSN
  • 0964-6906 (ISSN-L)
  • 1460-2083
OpenAlex
W2177880850
Cited by
66
References
77
Citations by year
2026: 2 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 5 · 2021: 10 · 2020: 7 · 2019: 8 · 2018: 7 · 2017: 5 · 2016: 6
FWCI
4.42
Type
journal article
Language
en
Open access
closed
Locations
  • Human Molecular Genetics (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Education, Culture, Sports, Science and Technology (MEXT) (26460921)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
tau protein, C-terminal fragment, tauopathy, aging, prion-like propagation, neurofibrillary tangles, calpain cleavage, tau aggregation, microtubule assembly, neurodegeneration
MeSH terms
Age Factors, Alzheimer Disease, Animals, Brain, Calpain, Cells, Cultured, Disease Models, Animal, Humans, Mice, Inbred C57BL, Mice, Transgenic, Microtubules, Phosphorylation, Prions, Neurofibrillary Tangles, tau Proteins, Protein Structure, Tertiary, Tauopathies, Mice

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