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40/100

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Down syndrome and Alzheimer's

Topic: Brain proteins, microglia and lab models

Hyperphosphorylation and dysregulation of exon 10 splicing of Tau are pivotally involved in pathogenesis of Alzheimer disease (AD) and/or other tauopathies. Alternative splicing of Tau exon 10, which encodes the second microtubule-binding repeat, generates Tau isoforms containing three and four microtubule-binding repeats, termed 3R-Taus and 4R-Taus, respectively. Dual specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A) lies at the Down syndrome critical region of chromosome 21. Overexpression of this kinase may contribute to the early Tau pathology in Down syndrome via phosphorylation of Tau and dysregulation of Tau exon 10. Here, we report that Dyrk1A was truncated at the C terminus and was associated with overactivation of calpain I in AD brain. Calpain I proteolyzed Dyrk1A in vitro first at the C terminus and further at the N terminus and enhanced its kinase activity toward Tau via increased Vmax but not Km. C-terminal truncation of Dyrk1A resulted in stronger activity than its full-length protein in promotion of exon 10 exclusion and phosphorylation of Tau. Dyrk1A was truncated in kainic acid-induced excitotoxic mouse brains and coincided with an increase in 3R-Tau expression and phosphorylation of Tau via calpain activation. Moreover, truncation of Dyrk1A was correlated with an increase in the ratio of 3R-Tau/4R-Tau and Tau hyperphosphorylation in AD brain. Collectively, these findings suggest that truncation/activation of Dyrk1A by Ca(2+)/calpain I might contribute to Tau pathology via promotion of exon 10 exclusion and hyperphosphorylation of Tau in AD brain.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Jin, N., Yin, X., Gu, J., Zhang, X., Shi, J., Qian, W., et al. (2015). Truncation and Activation of Dual Specificity Tyrosine Phosphorylation-regulated Kinase 1A by Calpain I: A MOLECULAR MECHANISM LINKED TO TAU PATHOLOGY IN ALZHEIMER DISEASE. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m115.645507

Vancouver

Jin N, Yin X, Gu J, Zhang X, Shi J, Qian W, et al. Truncation and Activation of Dual Specificity Tyrosine Phosphorylation-regulated Kinase 1A by Calpain I: A MOLECULAR MECHANISM LINKED TO TAU PATHOLOGY IN ALZHEIMER DISEASE. The Journal of biological chemistry. 2015. doi:10.1074/jbc.m115.645507. PMID: 25918155.

BibTeX

@article{jin2015-25918155,
  author  = {Jin, N. and Yin, X. and Gu, J. and Zhang, X. and Shi, J. and Qian, W. and Ji, Y. and Cao, M. and others},
  title   = {{Truncation and Activation of Dual Specificity Tyrosine Phosphorylation-regulated Kinase 1A by Calpain I: A MOLECULAR MECHANISM LINKED TO TAU PATHOLOGY IN ALZHEIMER DISEASE}},
  journal = {The Journal of biological chemistry},
  year    = {2015},
  doi     = {10.1074/jbc.m115.645507},
  pmid    = {25918155},
  url     = {https://doi.org/10.1074/jbc.m115.645507}
}

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Key findings

Here, we report that Dyrk1A was truncated at the C terminus and was associated with overactivation of calpain I in AD brain.
Collectively, these findings suggest that truncation/activation of Dyrk1A by Ca(2+)/calpain I might contribute to Tau pathology via promotion of exon 10 exclusion and hyperphosphorylation of Tau in AD brain.

Why it matters

In Alzheimer's disease brain, the kinase Dyrk1A was found to be truncated and overactivated by calpain I, which promoted tau exon 10 exclusion and tau hyperphosphorylation. This is a laboratory and animal study of a molecular mechanism and does not test any treatment in people.

Study details

Evidence strengthLow

How this study scored 40/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (The Journal of biological chemistry)
Journal's citation record	4 / 4	Journal of Biological Chemistry: journal h-index 780 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2015 — within 20 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	4 / 7	Cited 69 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	5.3 citations a year over 13 year(s) since 2015
Impact for its field and year	3 / 6	Cited 6.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	1 / 6	Cited by 2 other studies in this library
Still being cited	1 / 4	Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Fei Liu: h-index 59 (OpenAlex, whole career)
Institution's track record	0 / 3	Nantong University: institution h-index 261 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 25918155)
Free to read	0 / 2	Behind a paywall — scores zero
Total	40 / 100	—

What each of these 20 components measures, and what this score is not →

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