The molecule NCAM2, a glycoprotein from the superfamily of immunoglobulins, is a vital factor in the formation of the cerebral cortex, neuronal morphogenesis and formation of neuronal circuits in the brain, as stated in the new study published in the journal Cerebral Cortex. The deficit of NCAM2 causes an incorrect migration of neurons and alters the morphology, cytoskeleton and functionality of these cells in the central nervous system.
This article studies for the first time the activity of NCAM2 in the cortex and the hippocampus, brain structures where the function of this factor was so far unknown. The study is led by the experts Eduardo Soriano and Lluís Pujades, from the Faculty of Biology and the Institute of Neurosciences of the UB (UBNeuro), the Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED) and the Vall d’Hebron Research Institute (VHIR). The first author of the study is the researcher Antoni Parcerisas, member of the above-mentioned centers.
Other participants in this study are the experts from the Catalan Institution for Research and Advanced Studies (ICREA), Institute for Research in Biomedicine (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), the Spanish National Research Council (CSIC), the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) and the University of California in Davis (United States).
NCAM2: an unknown function in the cortex and hippocampus
The NCAM2 glycoprotein is a cell-adhesion molecule present in all vertebrates and which plays a decisive role in the organization of neuronal circuits in the central nervous system. This factor is largely expressed in the brain –from embryonic phases to adulthood- and specially in the olfactory bulb. Traditionally, all previous studies were focused on the olfactory bulb and proved a key role of the protein in neuronal synapses and neuronal compartmentalization between axons and dendrites. Recent studies described the involvement of NCAM2 in the formation and growth of neurites in cortical neurons, in the loss of synapsis in hippocampal neurons –caused by the amyloid peptide in Alzheimer’s disease- and the proliferation of neuronal progenitors in the spinal cord.
The new study describes for the first time the function of NCAM2 and the observed phenotypes in the development of the cortex and the hippocampus, a highly complex process regulated by many proteins. “In the study we confirm that a loss of NCAM2 creates an incorrect migration and position of neurons –these do not join the corresponding layer- and it also alters the neuronal morphology and the features of the cytoskeleton of nervous cells”, notes researcher Antoni Parcerisas.
“In the neuronal phenotype –adds Parcerisas- we see an altered dendritic tree –smaller and with many small and short dendrites- and an axon with more branches. In certain cases, some neurons show problems of neuronal polarization as well”.