Early N-Terminal Changes and Caspase-6 Cleavage of Tau in Alzheimer's Disease
Open accessAbstract
Alzheimer's disease (AD) is a progressive amnestic dementia that involves post-translational hyperphosphorylation, enzymatic cleavage, and conformational alterations of the microtubule-associated protein tau. The truncation state of tau influences many of its pathologic characteristics, including its ability to assume AD-related conformations and to assemble into filaments. Cleavage also appears to be an important marker in AD progression. Although C-terminal truncation of tau at D421 has recently been attributed to the apoptotic enzyme caspase-3, N-terminal processing of the protein remains mostly uncharacterized. Here, we report immunohistochemical staining in a cohort of 35 cases ranging from noncognitively impaired to early AD with a panel of three N-terminal anti-tau antibodies: Tau-12, 5A6, and 9G3-pY18. Of these three, the phosphorylation-independent epitope of 5A6 was the earliest to emerge in the pathological lesions of tau, followed by the appearance of the Tau-12 epitope. The unmasking of the Tau-12 epitope in more mature 5A6-positive tangles was not correlated with tau phosphorylation at tyrosine 18 (9G3-pY18). Still, later in the course of tangle evolution, the extreme N terminus of tau was lost, correlating temporally with the appearance of a C-terminal caspase-truncated epitope lacking residues 422-441. In addition, caspase-6 cleaved the N terminus of tau in vitro, preventing immunoreactivity with both Tau-12 and 5A6. Mass spectrometry confirmed that the in vitro caspase-6 truncation site is D13, a semicanonical and hitherto undescribed caspase cleavage site in tau. Collectively, these results suggest a role for caspase-6 and N-terminal truncation of tau during neurofibrillary tangle evolution and the progression of Alzheimer's disease.
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Tau can be cleaved by caspase-6 at Asp13 (tau-13) and Asp402 (tau-402).
“Tau can be cleaved by caspase-6 at Asp13 (tau-13) and Asp402 (tau-402) [193, 198].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [198]
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- Authors
- Horowitz, P. M., Patterson, K. R., Guillozet-Bongaarts, A. L., Reynolds, M. R., Carroll, C. A., Weintraub, S. T., Bennett, D. A., Cryns, V. L., Berry, R. W., & Binder, L. I.
- Affiliations
- Northwestern University (US)
- The University of Texas at San Antonio Health Science Center (US)
- Rush University (US)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-09-08
- Volume
- 24
- Issue
- 36
- Pages
- 7895-7902
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6729917
- OpenAlex
- W2137176838
- Cited by
- 215
- References
- 52
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 6 · 2023: 7 · 2022: 9 · 2021: 18 · 2020: 8 · 2019: 11 · 2018: 12 · 2017: 12 · 2016: 7 · 2015: 12 · 2014: 10 · 2013: 12 · 2012: 11
- FWCI
- 5.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5t32ag020418-08, AG09466, AG13854, AG10161, AG15819)
- National Institute on Aging (AG21661, AG20418, AG-15819, AG13854, AG 10161, R01AG021661, AG20506, AG09466, R01AG015819, P30AG010161, P01AG009466, P30AG013854, T32-AG020418, RF1AG015819, T32AG020506)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, tau protein, caspase-6, N-terminal truncation, neurofibrillary tangles, tau phosphorylation, apoptosis, disease progression
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Antibodies, Monoclonal, Antibody Specificity, Epitopes, Female, Humans, Male, Microscopy, Fluorescence, Nerve Tissue Proteins, Neurons, Protein Processing, Post-Translational, Proto-Oncogene Proteins, Recombinant Proteins, Temporal Lobe, Cohort Studies, Single-Blind Method, Neurofibrillary Tangles, tau Proteins, Apoptosis, Disease Progression, src-Family Kinases, Amino Acid Substitution, Caspases, Proto-Oncogene Proteins c-fyn, Caspase 6
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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