In the nervous system, astrocytes are organized to form a giant syncytium through gap junctions, which are intercellular membrane channels. This organization by gap junctions is rarely seen in mature neurons and provides the basis for the difference in function between astrocytes and neurons. Astrocytes use gap junctions to redistribute molecules[1]and, more importantly, to confer is potentiality on the syncytium[2], thus providing homeostatic function, including the clearance of elevated K+ and glutamate in extracellular space. Whether or how dysfunction of astrocytes syncytium causes neurological disorder is still uncertain despite extensive studies. This brief review focuses on recent neurological disorder findings and provides a view about is potentiality in an astrocytic syncytium and its relation to disorder based on these findings.

The current population is living longer than ever before as a result of improved health care services; therefore, the size of the ageing population is increasing [1]. Dementia is emerging as one of the main conditions affecting the elderly population. According to the WHO report, in 2010, there were approximately 35.6 million people suffering from dementia worldwide. This figure continues to rise, doubling approximately every 20 years and it is estimated that this will soon rise to 65.7 million by 2030, and further to 115.4 million by 2050. Current incidence shows an individual is diagnosed with dementia every four seconds. This has substantial socioeconomic and financial implications on people globally and the societal costs associated with disease were estimated at US$ 605 billion in 2010 [2].

Varicella is a high infectious disease with a worldwide distribution. According to a WHO position paper, global annual disease burden of Varicella is estimated to be 140 million cases [1]. Even if it is often considered a harmless disease, it may have a serious course and may require hospitalization. Among complications, neurological ones have been reported in previous studies. They may be caused by a primary infection or may be associated with a virus reactivation. Generally, children present with neurological complications associated to a primary infection. Those associated with recurrences are often due to the direct effect of viral replication in the central nervous system. Varicella zoster virus reaches the nervous system either through the bloodstream or by direct spread from sensory ganglia where it remains latent. The neurological consequences of Varicella reactivation are more frequent detached among elderly individuals and immunodeficient patients. Neurological involvement in immunocompetent children following Varicella reactivation is exceptionally rare. Varicella-zoster virus can infect a wide variety of cells in the central and peripheral nervous system, including neurons, oligodendrocytes, meningeal cells, ependymal cells, and cells of the blood vessel wall. The wide range of susceptible cells explains the diversity of the clinical and pathologic nervous system manifestations of VZV. The spectrum of VZV infection can range from mild symptomatic infection to meningoencephalitis.