Exp Neurobiol 2013; 22(4): 244-248
Published online December 30, 2013
© The Korean Society for Brain and Neural Sciences
Joongkyu Park1,2 and Kwang Chul Chung1*
1Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea, 2Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA
Correspondence to: *To whom correspondence should be addressed.
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Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS.
Keywords: down syndrome, Dyrk1A, neuritogenesis, synaptogenesis, cytoskeletal proteins