Early axonopathy preceding neurofibrillary tangles in mutant tau transgenic mice
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Neurodegenerative diseases characterized by brain and spinal cord involvement often show widespread accumulations of tau aggregates. We have generated a transgenic mouse line (Tg30tau) expressing in the forebrain and the spinal cord a human tau protein bearing two pathogenic mutations (P301S and G272V). These mice developed age-dependent brain and hippocampal atrophy, central and peripheral axonopathy, progressive motor impairment with neurogenic muscle atrophy, and neurofibrillary tangles and had decreased survival. Axonal spheroids and axonal atrophy developed early before neurofibrillary tangles. Neurofibrillary inclusions developed in neurons at 3 months and were of two types, suggestive of a selective vulnerability of neurons to form different types of fibrillary aggregates. A first type of tau-positive neurofibrillary tangles, more abundant in the forebrain, were composed of ribbon-like 19-nm-wide filaments and twisted paired helical filaments. A second type of tau and neurofilament-positive neurofibrillary tangles, more abundant in the spinal cord and the brainstem, were composed of 10-nm-wide neurofilaments and straight 19-nm filaments. Unbiased stereological analysis indicated that total number of pyramidal neurons and density of neurons in the lumbar spinal cord were not reduced up to 12 months in Tg30tau mice. This Tg30tau model thus provides evidence that axonopathy precedes tangle formation and that both lesions can be dissociated from overt neuronal loss in selected brain areas but not from neuronal dysfunction.
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Axonal degeneration precedes neuronal loss in mouse models of tauopathy and glaucoma.
“This alteration is an early event in tau-induced neuronal dysfunction and corroborates previous findings in mouse models of tautopathy and glaucoma, showing that axonal degeneration precedes neuronal loss (Schlamp et al., 2006; Leroy et al., 2007; Figure 1A, Table 1).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Leroy et al., 2007
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Ando, K., Nagaraj, S., Küçükali, F., de Fisenne, M.-A., Kosa, A.-C., Doeraene, E., Lopez Gutierrez, L., Brion, J.-P., & Leroy, K. (2022) · Cells · doi:10.3390/cells11243994 · Cited by 104 · see citing works
Self-citationLeroy, K., Ando, K., Héraud, C., Yilmaz, Z., Authelet, M., Boeynaems, J.-M., Buée, L., De Decker, R., & Brion, J.-P. (2010) · Journal of Alzheimer's Disease · doi:10.3233/jad-2010-1276 · Cited by 103 · see citing works
Self-citationHéraud, C., Goufak, D., Ando, K., Leroy, K., Suain, V., Yilmaz, Z., De Decker, R., Authelet, M., Laporte, V., Octave, J.-N., et al. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.09.010 · Cited by 80 · see citing works
Self-citationTauopathy contributes to synaptic and cognitive deficits in a murine model for Alzheimer’s disease
Stancu, I., Ris, L., Vasconcelos, B., Marinangeli, C., Goeminne, L., Laporte, V., Haylani, L. E., Couturier, J., Schakman, O., Gailly, P., et al. (2014) · The FASEB Journal · doi:10.1096/fj.13-246702 · Cited by 48 · see citing works
Selenica, M.-L. B., Davtyan, H., Housley, S. B., Blair, L. J., Gillies, A., Nordhues, B. A., Zhang, B., Liu, J., Gestwicki, J. E., Lee, D. C., et al. (2014) · Journal of Neuroinflammation · doi:10.1186/s12974-014-0152-0 · Cited by 40 · see citing works
- Authors
- Leroy, K., Bretteville, A., Schindowski, K., Gilissen, E., Authelet, M., De Decker, R., Yilmaz, Z., Buée, L., & Brion, J.-P.
- Affiliations
- Université Libre de Bruxelles (BE)
- Inserm (FR)
- Corresponding author
- Brion, Jean-Pierre
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2007-09
- Volume
- 171
- Issue
- 3
- Pages
- 976-992
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1959508
- OpenAlex
- W2047364115
- Cited by
- 135
- References
- 72
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 6 · 2023: 2 · 2022: 6 · 2021: 6 · 2020: 5 · 2019: 6 · 2018: 9 · 2017: 5 · 2016: 5 · 2015: 9 · 2014: 7 · 2013: 10 · 2012: 10
- FWCI
- 6.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Funders
- Fédération pour la Recherche sur le Cerveau
- Centre National de la Recherche Scientifique
- Agence Nationale de la Recherche (ANR-05-BLANC-0320-01)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tauopathy, neurofibrillary tangles, axonopathy, axonal swellings, axonal atrophy, neurofilaments, paired helical filaments, neuronal loss, motor impairment, neurogenic atrophy, stereology
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Animals, Atrophy, Axons, Brain, Inclusion Bodies, Disease Models, Animal, Humans, Mice, Transgenic, Motor Activity, Movement Disorders, Nerve Degeneration, Neurons, Sciatic Nerve, Spinal Cord, Neurofibrillary Tangles, tau Proteins, Neurofilament Proteins, Tauopathies, Glycogen Synthase Kinase 3, JNK Mitogen-Activated Protein Kinases, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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