Abstract

Synapses are sticky structures that physically connect neurons to one another as well as locations of cell-to-cell communication generated between the axons and dendrites of neurons. Synapse formation is hypothesized to be facilitated by a number of molecular processes, including cadherins and nectins. Calcium is necessary for the cadherin cell adhesion molecule. It has been shown that cadherins and catenins localize between axons and dendrites in neurons from the earliest stages of synaptogenesis. Cadherins affect how synapses form and change throughout time. In addition to cadherins, nectins are known to contribute to the construction and upkeep of intercellular adhesions. The brain expresses nectin-1,2 and 3. Here, the author reviews the specific effects of N-cadherin deletion on synapses and its relationship to diseases. Additionally, it has been discovered that nectin-1 and 3 play physiological roles in the development of synapses, alteration of mossy fibers' travel patterns, inter-neurite affinity, acquisition of contextual fear memory, and stress-related mental diseases. Nectin-2 has critical roles in the establishment of synapses as well as the homeostasis of astrocytes and neurons in the particular areas of the brain where it is generated. Additionally, a human NECTIN2 gene variant has been associated with Alzheimer's disease.

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