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44/100

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Down syndrome and Alzheimer's

Topic: Brain proteins, microglia and lab models

DYRK1A, dual-specificity tyrosine-regulated kinase 1A, maps to human chromosome 21 within the Down syndrome (DS) critical region. Dyrk1 phosphorylates the human microtubule-associated protein tau at Thr212 in vitro, a residue that is phosphorylated in fetal tau and hyper-phosphorylated in Alzheimer disease (AD) and tauopathies, including Pick disease (PiD). Furthermore, phosphorylation of Thr212 primes tau for phosphorylation by glycogen synthase kinase 3 (GSK-3). The present study examines Dyrk1A in the cerebral cortex of sporadic AD, adult DS with associated AD, and PiD. Increased Dyrk1A immunoreactivity has been found in the cytoplasm and nuclei of scattered neurons of the neocortex, entorhinal cortex, and hippocampus in AD, DS, and PiD. Dyrk1A is found in sarkosyl-insoluble fractions which are enriched in phosphorylated tau in AD brains, thus suggesting a possible association of Dyrk1A with neurofibrillary tangle pathology. Yet, no clear relationship has been observed between tau phosphorylation at Thr212, and GSK-3 and Dyrk1A expression in diseased brains. Transgenic mice bearing a triple tau mutation (G272V, P301L, and R406W) and expressing hyper-phosphoyrylated tau in neurons of the entorhinal cortex, hippocampus, and cerebral neocortex show increased expression of Dyrk1A in individual neurons in the same regions. However, transgenic mice over-expressing Dyrk1A do not show increased phosphorylation of tau at Thr212, thus suggesting that Dyrk1A over-expression does not trigger per se hyper-phosphorylation of tau at Thr212 in vivo. The present observations indicate modifications in the expression of constitutive Dyrk1A in the cytoplasm and nuclei of neurons in various neurodegenerative diseases associated with tau phosphorylation.

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

APA 7th

Ferrer, I., Barrachina, M., Puig, B., Martínez de Lagrán, M., Martí, E., Avila, J., et al. (2005). Constitutive Dyrk1A is abnormally expressed in Alzheimer disease, Down syndrome, Pick disease, and related transgenic models. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2005.03.020

Vancouver

Ferrer I, Barrachina M, Puig B, Martínez de Lagrán M, Martí E, Avila J, et al. Constitutive Dyrk1A is abnormally expressed in Alzheimer disease, Down syndrome, Pick disease, and related transgenic models. Neurobiology of disease. 2005. doi:10.1016/j.nbd.2005.03.020. PMID: 16242644.

BibTeX

@article{ferrer2005-16242644,
  author  = {Ferrer, I. and Barrachina, M. and Puig, B. and Martínez de Lagrán, M. and Martí, E. and Avila, J. and Dierssen, M.},
  title   = {{Constitutive Dyrk1A is abnormally expressed in Alzheimer disease, Down syndrome, Pick disease, and related transgenic models}},
  journal = {Neurobiology of disease},
  year    = {2005},
  doi     = {10.1016/j.nbd.2005.03.020},
  pmid    = {16242644},
  url     = {https://doi.org/10.1016/j.nbd.2005.03.020}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

Key findings

However, transgenic mice over-expressing Dyrk1A do not show increased phosphorylation of tau at Thr212, thus suggesting that Dyrk1A over-expression does not trigger per se hyper-phosphorylation of tau at Thr212 in vivo.
The present observations indicate modifications in the expression of constitutive Dyrk1A in the cytoplasm and nuclei of neurons in various neurodegenerative diseases associated with tau phosphorylation.

Why it matters

This study found altered Dyrk1A expression in neurons in Alzheimer disease, Down syndrome and Pick disease, and in a transgenic mouse model, but mice over-expressing Dyrk1A did not show increased tau phosphorylation at Thr212. It describes a possible disease association and reports no treatment or cure.

Study details

Evidence strengthLow

How this study scored 44/100

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

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Neurobiology of disease)
Journal's citation record	2 / 4	Neurobiology of Disease: journal h-index 225 (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	2005 — older than 20 years, still counted
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	Laboratory or animal study (title names “transgenic”) — scores zero
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 178 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	7.7 citations a year over 23 year(s) since 2005
Impact for its field and year	3 / 6	Cited 3.8× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 14 other studies in this library
Still being cited	2 / 4	Cited 23 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Mara Dierssen: h-index 61 (OpenAlex, whole career)
Institution's track record	1 / 3	Universidad Autónoma de Madrid: institution h-index 709 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 5 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 16242644)
Free to read	0 / 2	Behind a paywall — scores zero
Total	44 / 100	—

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