PMU-Autor/inn/en
Aigner LudwigAbstract
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