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Current Molecular Medicine

Editor-in-Chief

ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

Molecular Mechanisms of Neuronal Migration Disorders, Quo Vadis?

Author(s): S. Couillard-Despres, J. Winkler, G. Uyanik and L. Aigner

Volume 1, Issue 6, 2001

Page: [677 - 688] Pages: 12

DOI: 10.2174/1566524013363195

Price: $65

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.

Keywords: Neuronal Migration Disorders, Quo Vadis, Cell Proliferation, Magnetic resonance imaging, Microtubule-organizing center, Positron emission tomography, Subcortical laminar heterotopia, Periventricular nodular heterotopia


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