Next Article in Journal
Early Senescence and Leukocyte Telomere Shortening in SCHIZOPHRENIA: A Role for Cytomegalovirus Infection?
Previous Article in Journal
Optimising Outcomes for Glioblastoma through Subspecialisation in a Regional Cancer Centre
Article Menu
Issue 10 (October) cover image

Export Article

Open AccessReview
Brain Sci. 2018, 8(10), 187; https://doi.org/10.3390/brainsci8100187

DYRK1A Protein, A Promising Therapeutic Target to Improve Cognitive Deficits in Down Syndrome

1
Service de gynécologie obstétrique, HFR Fribourg-Hôpital cantonal, Chemin des Pensionnats 2-6, Case Postale, 1708 Fribourg, Switzerland
2
Department of Genetic Medicine and Development, University of Geneva Medical School and Geneva University Hospitals, 1 rue Michel-Servet, 1211 Geneva, Switzerland
*
Author to whom correspondence should be addressed.
Received: 4 September 2018 / Revised: 24 September 2018 / Accepted: 11 October 2018 / Published: 16 October 2018
Full-Text   |   PDF [623 KB, uploaded 16 October 2018]   |  

Abstract

Down syndrome (DS) caused by a trisomy of chromosome 21 (HSA21), is the most common genetic developmental disorder, with an incidence of 1 in 800 live births. Its phenotypic characteristics include intellectual impairment, early onset of Alzheimer’s disease, congenital heart disease, hypotonia, muscle weakness and several other developmental abnormalities, for the majority of which the pathogenetic mechanisms remain unknown. Among the numerous protein coding genes of HSA21, dual-specificity tyrosine-(Y)-phosphorylation-regulated kinase 1A (DYRK1A) encodes a proline-directed serine/threonine and tyrosine kinase that plays pleiotropic roles in neurodevelopment in both physiological and pathological conditions. Numerous studies point to a crucial role of DYRK1A protein for brain defects in patients with DS. Thus, DYRK1A inhibition has shown benefits in several mouse models of DS, including improvement of cognitive behaviour. Lastly, a recent clinical trial has shown that epigallocatechine gallate (EGCG), a DYRK1A inhibitor, given to young patients with DS improved visual recognition memory, working memory performance and adaptive behaviour. View Full-Text
Keywords: down syndrome; trisomy 21; DYRK1A; cognitive impairment; therapy down syndrome; trisomy 21; DYRK1A; cognitive impairment; therapy
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Feki, A.; Hibaoui, Y. DYRK1A Protein, A Promising Therapeutic Target to Improve Cognitive Deficits in Down Syndrome. Brain Sci. 2018, 8, 187.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Brain Sci. EISSN 2076-3425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top