Cited by 194Down syndrome and intellectual disability researchGenetics and Neurodevelopmental DisordersWilliams Syndrome Research

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Trisomy-driven overexpression of DYRK1A kinase in the brain of subjects with Down syndrome

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Dowjat, Wieslaw K., Adayev, Tatyana, Kuchna, Izabela, Nowicki, Krzysztof, Palminiello, Sonia, Hwang, Yu Wen, Wegiel, Jerzy·2007·Neuroscience Letters

DOI 10.1016/j.neulet.2006.11.026PMC PMC1890010

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Abstract

Down syndrome (DS) is the most common genetic disorder associated with mental retardation (MR). It is believed that many of the phenotypic features of DS stem from enhanced expression of a set of genes located within the triplicated region on chromosome 21. Among those genes is DYRK1A encoding dual-specificity proline-directed serine/treonine kinase, which, as documented by animal studies, can potentially contribute to cognitive deficits in DS. Whether this contribution can be exerted through elevated levels of DYRK1A protein in the brain of DS subjects was the main goal of the present study. The levels of DYRK1A protein were measured by Western blotting in six brain structures that included cerebral and cerebellar cortices and white matter. The study involved large cohorts of DS subjects and age-matched controls representing infants and adults of different age, gender and ethnicity. Trisomic Ts65Dn mice, an animal model of DS, were also included in the study. Both in trisomic mice and in DS subjects, the brain levels of DYRK1A protein were increased approximately 1.5-fold, indicating that this protein is overexpressed in gene dosage-dependent manner. The exception was an infant group, in which there was no enhancement suggesting the existence of a developmentally regulated mechanism. We found DYRK1A to be present in every analyzed structure irrespective of age. This widespread occurrence and constitutive expression of DYRK1A in adult brain suggest an important, but diverse from developmental role played by this kinase in adult central nervous system. It also implies that overexpression of DYRK1A in DS may be potentially relevant to MR status of these individuals during their entire life span.

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Authors: Dowjat, W. K., Adayev, T., Kuchna, I., Nowicki, K., Palminiello, S., Hwang, Y. W., & Wegiel, J.
Affiliations: IRCCS San Raffaele Roma (IT)
Corresponding author: Dowjat, Wieslaw K.
ORCID: Dowjat, Wieslaw K.
Nowicki, Krzysztof
Venue: Neuroscience Letters
Publisher: Elsevier BV
Published: 2007-02
Volume: 413
Issue: 1
Pages: 77-81
ISSN: 0304-3940 (ISSN-L)
DOI: 10.1016/j.neulet.2006.11.026
PMC: PMC1890010
OpenAlex: W1964178482
Cited by: 190
References: 32
Citations by year: 2026: 4 · 2025: 5 · 2024: 5 · 2023: 14 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 7 · 2018: 9 · 2017: 14 · 2016: 9 · 2015: 12 · 2014: 11 · 2013: 8 · 2012: 17
FWCI: 9.36
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience Letters (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD043960, R01 HD43960, R01HD38295, R01HD038295)
Topics: Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Life Sciences › Neuroscience › Developmental Neuroscience › Williams Syndrome Research
Keywords: Down syndrome, DYRK1A, gene dosage, protein overexpression, brain, intellectual disability, Ts65Dn mouse model, developmental regulation, adult central nervous system
MeSH terms: Dyrk Kinases, Adolescent, Adult, Age Factors, Aged, Animals, Child, Child, Preschool, Chromosomes, Human, Pair 21, Down Syndrome, Humans, Infant, Mice, Transgenic, Middle Aged, Protein-Tyrosine Kinases, Trisomy, Case-Control Studies, Protein Serine-Threonine Kinases, Gene Expression Regulation, Developmental, Mice

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Trisomy-driven overexpression of DYRK1A kinase in the brain of subjects with Down syndrome

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