The DOI matches its Crossref record; 206 of the 206 references it cites were found in a registry or an index.
Axonal Degeneration in Tauopathies: Disease Relevance and Underlying Mechanisms
Open accessAbstract
Tauopathies are a diverse group of diseases featuring progressive dying back neurodegeneration of specific neuronal populations in association with accumulation of abnormal forms of the microtubule-associated protein tau. It is well established that the clinical symptoms characteristic of tauopathies correlate with deficits in synaptic function and neuritic connectivity early in the course of disease, but mechanisms underlying these critical pathogenic events remain largely unknown. Biochemical in vitro evidence fueled the widespread notion that microtubule stabilization represents tau’s primary biological role and that the marked atrophy of neurites observed in tauopathies results from loss of microtubule stability. However, this notion contrasts with the mild phenotype associated with tau deletion. Instead, an analysis of cellular hallmarks common to different tauopathies, including aberrant patterns of protein phosphorylation and early degeneration of axons, suggests that alterations in kinase-based signaling pathways and deficits in axonal transport associated with such alterations contribute to the loss of neuronal connectivity triggered by pathogenic forms of tau. Here, we review a body of literature providing evidence that axonal pathology represents an early and common pathogenic event among human tauopathies. Observations of axonal degeneration in animal models of specific tauopathies are discussed and similarities to human disease highlighted. Finally, we discuss potential mechanistic pathways other than microtubule destabilization by which disease-related forms of tau may promote axonopathy.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The dose for this experiment was chosen based upon previous work by Brunden et. al. and Zhang et. al. in which EpoD at 1mg/kg was sufficient to reduce measures of tauopathy, neurodegeneration and axonal dystrophy in PS19 tau mice 30, 31.”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [31]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Additionally, previous studies utilizing EpoD as well as microtubule-stabilizing peptide NAP have both shown ability to reduce p-tau pathology in AD model mice over several months of treatment 31,66,67”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [31]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Data from previous studies have found evidence that EpoD can promote axonal health by reducing axonal dystrophy, increasing ON microtubule density and normalizing fast axonal transport 30, 31.”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [31]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Items 201–206 of 206
Braak, E., Arai, K., & Braak, H. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7131 · Cited by 21
Nakamura, Y., Takeda, M., Yoshimi, K., Hattori, H., Hariguchi, S., Hashimoto, S., & Nishimura, T. (1994) · Neuroscience Letters · doi:10.1016/0304-3940(94)90905-9 · Cited by 18
Hebron, M. L., Algarzae, N. K., Lonskaya, I., & Moussa, C. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2013.01.009 · Cited by 14
Wang, L., Zhu, M., Feng, Y., & Wang, J. (2006) · Neuropathology · doi:10.1111/j.1440-1789.2006.00671.x · Cited by 10
Pathological and biochemical studies on a case of Pick disease with severe white matter atrophy
Yamakawa, K., Takanashi, M., Watanabe, M., Nakamura, N., Kobayashi, T., Hasegawa, M., Mizuno, Y., Tanaka, S., & Mori, H. (2006) · Neuropathology · doi:10.1111/j.1440-1789.2006.00738.x · Cited by 4
Flagged first, then by citations
Cited by
Sorted by citations
Kinetically distinct phases of tau on microtubules regulate kinesin motors and severing enzymes
Siahaan, V., Krattenmacher, J., Hyman, A. A., Diez, S., Hernández-Vega, A., Lansky, Z., & Braun, M. (2019) · Nature Cell Biology · doi:10.1038/s41556-019-0374-6 · Cited by 169
GSK3β and tau protein in Alzheimer's disease and epilepsy
Toral-Rios, D., Pichardo-Rojas, P. S., Alonso-Vanegas, M., & Campos-Peña, V. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00019 · Cited by 158
New Insights Into Drug Discovery Targeting Tau Protein
Soeda, Y., & Takashima, A. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.590896 · Cited by 136
Zavaliangos-Petropulu, A., Nir, T. M., Thomopoulos, S. I., Reid, R. I., Bernstein, M. A., Borowski, B., Jack Jr., C. R., Weiner, M. W., Jahanshad, N., & Thompson, P. M. (2019) · Frontiers in Neuroinformatics · doi:10.3389/fninf.2019.00002 · Cited by 101
“…of amyloid plaques and neurofibrillary tangles (NFTs) in the brain (Braak and Braak, 1991, 1996; Frank et al., 2003; Shaw et al., 2007) can directly impact WM (Lee et al., 2004; Roth et al., 2005), promoting myelin degeneration and axonal loss (Braak and Braak, 1996; Kneynsberg et al., 2017).”
Akbar, M., Shabbir, A., Rehman, K., Akash, M. S. H., & Shah, M. A. (2021) · Journal of Food Biochemistry · doi:10.1111/jfbc.13936 · Cited by 97
Metadata
- Authors
- Kneynsberg, A., Combs, B., Christensen, K., Morfini, G., & Kanaan, N. M.
- Affiliations
- Michigan State University (US)
- University of Illinois Chicago (US)
- Trinity Health Grand Rapids (US)
- Corresponding author
- Morfini, Gerardo
- Kanaan, Nicholas M.
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2017-10-17
- Volume
- 11
- Pages
- 572-572
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC5651019
- OpenAlex
- W2763441547
- Cited by
- 102
- References
- 206
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 8 · 2023: 6 · 2022: 15 · 2021: 18 · 2020: 18 · 2019: 16 · 2018: 8
- FWCI
- 1.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (R01 AG044372)
- National Institute of Neurological Disorders and Stroke (R01 NS082730, R21 NS096642, R01 NS066942)
- BrightFocus Foundation (A2013364S)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tauopathy, axonal degeneration, axonopathy, tau protein, microtubule stabilization, microtubule destabilization, tau phosphorylation, kinase signaling pathways, axonal transport, neuronal connectivity, dying-back degeneration
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 ›
Are you an author, or do you see a problem with this page? Request a review
