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      Contactins in the central nervous system: role in health and disease

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          Abstract

          Contactins are a group of cell adhesion molecules that are mainly expressed in the brain and play pivotal roles in the organization of axonal domains, axonal guidance, neuritogenesis, neuronal development, synapse formation and plasticity, axo-glia interactions and neural regeneration. Contactins comprise a family of six members. Their absence leads to malformed axons and impaired nerve conduction. Contactin mediated protein complex formation is critical for the organization of the axon in early central nervous system development. Mutations and differential expression of contactins have been identified in neuro-developmental or neurological disorders. Taken together, contactins are extensively studied in the context of nervous system development. This review summarizes the physiological roles of all six members of the Contactin family in neurodevelopment as well as their involvement in neurological/neurodevelopmental disorders.

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          Most cited references 127

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          Biology of oligodendrocyte and myelin in the mammalian central nervous system.

          Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the proteolipid protein, which lead to dysmyelinating diseases in animals and human (jimpy mutation and Pelizaeus-Merzbacher disease or spastic paraplegia, respectively). Oligodendrocytes, as astrocytes, are able to respond to changes in the cellular and extracellular environment, possibly in relation to a glial network. There is also a remarkable plasticity of the oligodendrocyte lineage, even in the adult with a certain potentiality for myelin repair after experimental demyelination or human diseases.
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            Vision in autism spectrum disorders.

            Autism spectrum disorders (ASDs) are developmental disorders which are thought primarily to affect social functioning. However, there is now a growing body of evidence that unusual sensory processing is at least a concomitant and possibly the cause of many of the behavioural signs and symptoms of ASD. A comprehensive and critical review of the phenomenological, empirical, neuroscientific and theoretical literature pertaining to visual processing in ASD is presented, along with a brief justification of a new theory which may help to explain some of the data, and link it with other current hypotheses about the genetic and neural aetiologies of this enigmatic condition.
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              Identifying autism loci and genes by tracing recent shared ancestry.

              To find inherited causes of autism-spectrum disorders, we studied families in which parents share ancestors, enhancing the role of inherited factors. We mapped several loci, some containing large, inherited, homozygous deletions that are likely mutations. The largest deletions implicated genes, including PCDH10 (protocadherin 10) and DIA1 (deleted in autism1, or c3orf58), whose level of expression changes in response to neuronal activity, a marker of genes involved in synaptic changes that underlie learning. A subset of genes, including NHE9 (Na+/H+ exchanger 9), showed additional potential mutations in patients with unrelated parents. Our findings highlight the utility of "homozygosity mapping" in heterogeneous disorders like autism but also suggest that defective regulation of gene expression after neural activity may be a mechanism common to seemingly diverse autism mutations.
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                Author and article information

                Journal
                Neural Regen Res
                Neural Regen Res
                NRR
                Neural Regeneration Research
                Medknow Publications & Media Pvt Ltd (India )
                1673-5374
                1876-7958
                February 2019
                : 14
                : 2
                : 206-216
                Affiliations
                [1 ]Amsterdam UMC, VU University Medical Center, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam, The Netherlands
                [2 ]Institute of Neurophysiology and Cellular Biophysics, University of Göttingen, Göttingen, Germany
                [3 ]DFG Research Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), University of Göttingen, Göttingen, Germany
                [4 ]DFG Excellence Cluster 171, University of Göttingen, Göttingen, Germany
                Author notes
                [* ] Correspondence to: Charlotte E. Teunissen, c.teunissen@ 123456vumc.nl .

                Author contributions: Manuscript writing: MC; content review: DS and CET.

                Article
                NRR-14-206
                10.4103/1673-5374.244776
                6301169
                30530999
                Copyright: © Neural Regeneration Research

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

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