Neuroinflammation is an important physiological consideration when investigating the etiology of schizophrenia; however, limited and ambiguous data exist on this phenomenon. This is a fundamental limitation to understanding the etiology of schizophrenia and determining treatment rationales. Thus, neuroinflammation offers important insights into the bidirectional association between the central nervous system and the immune system (O’Connor, Moynihan, & Castera, 2014). However, confounds exist in the literature that question the relationship between neuroinflammation and white matter pathology when attempting to discern the etiology of schizophrenia (Doorduin, de Vries, Willemsen, de Groot, Dierckx, & Klein, 2009). Therefore, this paper considers …show more content…
Various findings across studies suggest that neuroinflammation is implicated in white matter pathology and is characterized by reduced density of astroglia and oligodendroglia, and increased density of microglia; in turn, leading to axonal degeneration, myelin breakdown (Chew, Fusar-Poli, & Schmitz, 2013). According to Doorduin et al. (2009), microglial cells are implicated in the removal of irreversibly damaged brain tissue. Thus, it is hypothesized that the chronic activation of microglia is derived from neuroinflammatory processes (Doorduin et al., 2009). Moreover, according to Najjar & Pearlman (2015), when microglia become chronically activated detrimental effects occur, including structural and functional disconnectivity of white matter tracts. Additionally, Hercher et al. (2014) also observed volume reductions in oligodendrocytes and astrocytes that may reflect compromised white matter integrity in individuals with schizophrenia. Thus, the aberrations in white matter glia and the alterations in axons, both structurally and functionally, contribute to the disturbed neural connectivity observed in individuals with schizophrenia (Hercher et al., 2014; Najjar et al.,