Molecular mechanisms of neuronal migration disorders, quo vadis?

Current Molecular Medicine
S Couillard-DespresL Aigner

Abstract

Following terminal mitosis, neuronal precursor cells leave their site of origin and migrate towards their definitive site of residency. In order to establish the intricate cytoarchitecture described in the adult human brain, neuronal migration must be finely regulated. In humans, brain malformations can result from neuronal migration defects. The spectrum of migration disorder severity extends from few heterotopic neurons, as observed in periventricular heterotopia, to a complete cortical disorganization, as observed in cases of lissencephaly. Recently, specific migration disorders have been linked to mutations/deletions in the doublecortin, filamin-1, LIS1 and reelin genes. These proteins act at different levels of the signaling cascades transducing extracellular guiding cues into cytoskeletal reorganization. Here, we summarize the data concerning these four molecules and speculate on their functions and interaction partners during neuronal development.

Citations

Mar 31, 2004·Experimental Eye Research·Maren EngelhardtLudwig Aigner
Nov 28, 2012·The British Journal of Nutrition·Hyo Geun Kim, Myung Sook Oh
Jan 19, 2005·The European Journal of Neuroscience·Sebastien Couillard-DespresLudwig Aigner
Feb 8, 2006·Neurosurgical Focus·Vincent Y WangNicholas M Barbaro
Feb 6, 2014·Neurosurgical Review·Dario J Englot, Edward F Chang
Jan 1, 2009·Fetal and Pediatric Pathology·Thora S SteffensenCurtis E Margo
Jan 25, 2005·Journal of Neurochemistry·Claudia KarlLudwig Aigner
Oct 24, 2003·The Journal of Comparative Neurology·Jason P BrownH Georg Kuhn
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Mar 15, 2015·Developmental Biology·Crystal E Love, Victoria E Prince
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Jan 25, 2020·Journal of Neural Transmission·Aline SiteneskiAna Lúcia S Rodrigues

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