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Forschungsdatenbank PMU-SQQUID

Molecular mechanisms of neuronal migration disorders, quo vadis?
Couillard-Despres, S; Winkler, J; Uyanik, G; Aigner, L;
Curr Mol Med. 2001; 1(6): 677-688.
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PMU-Autor/inn/en

Aigner Ludwig
Couillard-Després Sébastien

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.


Useful keywords (using NLM MeSH Indexing)

1-Alkyl-2-acetylglycerophosphocholine Esterase

Animals

Brain/abnormalities*

Brain/embryology

Brain/pathology

Cell Adhesion Molecules, Neuronal/genetics

Cell Division

Cell Movement/genetics

Cell Movement/physiology

Cerebral Cortex/embryology

Contractile Proteins/genetics

Extracellular Matrix Proteins/genetics

Humans

Microfilament Proteins/genetics

Microtubule-Associated Proteins/genetics

Mutation

Nerve Tissue Proteins

Neurons/pathology

Neurons/physiology*

Neuropeptides/genetics

Serine Endopeptidases

Signal Transduction