The DOI matches its Crossref record; 250 of the 250 references it cites were found in a registry or an index.
Tau pathology and neurodegeneration
Abstract
The pathway leading from soluble and monomeric to hyperphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenerative diseases, collectively referred to as tauopathies. Dominantly inherited mutations in MAPT, the gene that encodes tau, cause forms of frontotemporal dementia and parkinsonism, proving that dysfunction of tau is sufficient to cause neurodegeneration and dementia. However, most cases of tauopathy are not inherited in a dominant manner. The first tau aggregates form in a few nerve cells in discrete brain areas. These become self propagating and spread to distant brain regions in a prion-like manner. The prevention of tau aggregation and propagation is the focus of attempts to develop mechanism-based treatments for tauopathies.
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“Aggregates composed of both 3R and 4R tau are seen in disease states, though curiously several tauopathies including PSP, CBD, FTDP-17, and AGD exclusively feature 4R tau deposits.”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [1]
In the citing paper
“Pathological studies have shown the deposition of abnormal proteins in the brain tissues of FTD patients, including TDP-43 (50% of cases), tau (40% of cases), and FUS (5–10% of cases).314,315”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [315]
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1 retracted
Larson, M. E., Sherman, M. A., Amar, F., Nuvolone, M., Schneider, J. A., Bennett, D. A., Aguzzi, A., & Lesné, S. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.1858-12.2012 · Cited by 290
RetractedNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Glenner, G. G., & Wong, C. W. (1984) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(84)80190-4 · Cited by 5,404
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.82.12.4245 · Cited by 4,431
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Clinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814
Grundke-Iqbal, I., Iqbal, K., Tung, Y. C., Quinlan, M., Wisniewski, H. M., & Binder, L. I. (1986) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.83.13.4913 · Cited by 3,676
Research works printed but not linked: 4
- Alzheimer, 1907, On a peculiar disease of the cerebral cortex, Allg Z Psychiat, 64, 146
- Fischer, 1907, Miliary necroses with geodic proliferations of the neurofibrils, a regular change of the cerebral cortex in senile dementia, Monatsschr Psychiat Neurol, 22, 361
- Brion, 1985, Immunological detection of tau protein in the lesions of the neurofibrillary degeneration of Alzheimer's disease, Arch Biol (Bruxelles), 95, 229
- Wilson, 1997, Free fatty acids stimulate the polymerization of tau and amyloid beta peptides, Am J Pathol, 150, 2181
Cited by
Sorted by citations
Ageing as a risk factor for neurodegenerative disease
Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0244-7 · Cited by 3,310
Fang, E. F., Hou, Y., Palikaras, K., Adriaanse, B. A., Kerr, J. S., Yang, B., Lautrup, S., Hasan-Olive, M. M., Caponio, D., Dan, X., et al. (2019) · Nature Neuroscience · doi:10.1038/s41593-018-0332-9 · Cited by 1,740
Pathology of Neurodegenerative Diseases
Dugger, B. N., & Dickson, D. W. (2017) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a028035 · Cited by 1,665
Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets
Gao, C., Jiang, J., Tan, Y., & Chen, S. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01588-0 · Cited by 1,616
The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans
Holth, J. K., Fritschi, S. K., Wang, C., Pedersen, N. P., Cirrito, J. R., Mahan, T. E., Finn, M. B., Manis, M., Geerling, J. C., Fuller, P. M., et al. (2019) · Science · doi:10.1126/science.aav2546 · Cited by 813
Metadata
- Authors
- Spillantini, M. G., & Goedert, M.
- Affiliations
- University of Cambridge (GB)
- MRC Laboratory of Molecular Biology (GB)
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 12
- Issue
- 6
- Pages
- 609-622
- ISSN
- 1474-4422 (ISSN-L)
- OpenAlex
- W2137140827
- Cited by
- 1,133
- References
- 250
- Citations by year
- 2026: 60 · 2025: 89 · 2024: 69 · 2023: 78 · 2022: 97 · 2021: 102 · 2020: 99 · 2019: 113 · 2018: 87 · 2017: 89 · 2016: 80 · 2015: 88 · 2014: 60 · 2013: 19
- FWCI
- 9.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Parkinson's UK (K-1012)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tau pathology, tauopathy, neurodegeneration, tau aggregation, hyperphosphorylated tau, MAPT mutations, frontotemporal dementia, parkinsonism, prion-like propagation, tau-targeted therapy
- MeSH terms
- Animals, Brain, Humans, tau Proteins, Neurodegenerative Diseases, Tauopathies
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