Cited by 281Alzheimer's disease research and treatmentsDown syndrome and intellectual disability researchDementia and Cognitive Impairment Research

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome

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Liu, Fei, Liang, Zhihou, Wegiel, Jerzy, Hwang, Yu‐Wen, Iqbal, Khalid, Grundke‐Iqbal, Inge, Ramakrishna, Narayan, Gong, Cheng‐Xin·2008·The FASEB Journal

DOI 10.1096/fj.07-104539PMC PMC2518253

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Abstract

Adults with Down syndrome (DS) develop Alzheimer neurofibrillary degeneration in the brain, but the underlying molecular mechanism is unknown. Here, we report that the presence of an extra copy of the dual‐specificity tyrosine‐phosphorylated and regulated kinase 1A ( Dyrk1A ) gene due to trisomy 21 resulted in overexpression of Dyrk1A and elevated kinase activity in DS brain. Dyrk1A phosphorylated tau at several sites, and these sites were hyperphosphory‐lated in adult DS brains. Phosphorylation of tau by Dyrk1A primed its further phosphorylation by glycogen synthase kinase‐3β (GSK‐3β). Dyrk1A‐induced tau phosphorylation inhibited tau's biological activity and promoted its self‐aggregation. In Ts65Dn mouse brain, an extra copy of the Dyrk1A gene caused increased expression and activity of Dyrk1A and resulted in increased tau phosphorylation. These findings strongly suggest a novel mechanism by which the overexpression of Dyrk1A in DS brain causes neurofibrillary degeneration via hyperphosphorylating tau. Liu, F., Liang, Z., Wegiel, J., Hwang, Y.‐W., Iqbal, K., Grundke‐Iqbal, I., Ramakrishna, N., Gong, C.‐X. Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome. FASEB J. 22, 3224–3233 (2008)

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BindingDB Entry 50018847: Silmitasertib (CX-4945), a Clinically Used CK2-Kinase Inhibitor with Additional Effects on GSK3β and DYRK1A Kinases: A Structural Perspective.
BindingDB (2024) · UC San Diego · doi:10.7270/q2d79gng
BindingDB Entry 50016416: Structure-Activity Relationship in the Leucettine Family of Kinase Inhibitors.
BindingDB (2023) · UC San Diego · doi:10.7270/q2fn1b7v
UNDERSTANDING THE FUNCTION OF DYRK1A THROUGH CHARACTERIZATION OF ITS INTERACTING PROTEINS
Ananthapadmanabhan, V. (2015) · VCU Scholars Compass (Virginia Commonwealth University) · doi:10.25772/n51j-0z89
Mosaicism for trisomy21: Utility of array-based technology for its detection and its influence on telomere length and the frequency of acquired chromosome abnormalities
Charalsawadi, C. (2011) · VCU Scholars Compass (Virginia Commonwealth University) · doi:10.25772/yfrf-z457
Down Syndrome: Neuropsychological phenotype and mitochondrial DNA
Lomartire, L. (2012) · AMS Dottorato Institutional Doctoral Theses Repository (University of Bologna) · doi:10.6092/unibo/amsdottorato/4552

Authors: Liu, F., Liang, Z., Wegiel, J., Hwang, Y., Iqbal, K., Grundke‐Iqbal, I., Ramakrishna, N., & Gong, C.
Affiliations: Department of Neurochemistry New York State Institute for Basic Research in Developmental Disabilities Staten Island New York USA
Department of Developmental Neurobiology New York State Institute for Basic Research in Developmental Disabilities Staten Island New York USA
Department of Molecular Biology New York State Institute for Basic Research in Developmental Disabilities Staten Island New York USA
ORCID: Liang, Zhihou
Hwang, Yu‐Wen
Iqbal, Khalid
Gong, Cheng‐Xin
Venue: The FASEB Journal
Publisher: Wiley
Published: 2008-05-28
Volume: 22
Issue: 9
Pages: 3224-3233
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.07-104539
PMC: PMC2518253
OpenAlex: W1986503994
Cited by: 272
References: 62
Citations by year: 2026: 19 · 2025: 16 · 2024: 18 · 2023: 17 · 2022: 20 · 2021: 18 · 2020: 13 · 2019: 13 · 2018: 11 · 2017: 23 · 2016: 8 · 2015: 11 · 2014: 15 · 2013: 16 · 2012: 9
FWCI: 10.19
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (AG027429, HD043960, HD038295, AG019158)
Alzheimer's Association (IIRG-05-13095)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: DYRK1A, Down syndrome, neurofibrillary degeneration, tau hyperphosphorylation, glycogen synthase kinase-3β, kinase activity, Ts65Dn mouse model, Alzheimer's disease
MeSH terms: Glycogen Synthase Kinase 3 beta, Dyrk Kinases, Aged, Aged, 80 and over, Animals, Down Syndrome, Female, Humans, Male, Middle Aged, Nerve Degeneration, Phosphorylation, Protein-Tyrosine Kinases, Neurofibrillary Tangles, tau Proteins, Protein Serine-Threonine Kinases, Gene Expression Regulation, Developmental, Glycogen Synthase Kinase 3, Mice

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome

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