SCHIZOPHRENIA AND OLFACTORY DISFUNCTION: NEUROIMAGING INSIGHTS TOWARD AN EARLY DEVELOPMENT DISRUPTION

Olfactory dysfunction (OD) is relatively specific to schizophrenia (SZ) and its negative symptoms (Schecklmann et al., 2013). Similarly to what is known for Alzheimer Disease, OD identification may predict transition to clinical disorder in high-risk individuals for SZ, being potentially one of the most viable risk biomarkers identified (Turetsky et al, 2012). Research suggests that abnormalities in SZ extend to more peripheral olfactory structures including neuroepithelial dysfunctional processes (Rupp, 2010). Olfactory bulb mitral cells synapses with neuroepithelium, retrieving information throughout the olfactory tract to primary olfactory areas and other regions involved in crucial functions impaired in SZ, such as emotion regulation and executive planning, namely amygdala, hippocampus or orbitofrontal cortex. Olfactory bulb and olfactory tract lay bellow the basal forebrain, modeling the olfactory sulcus. MRI findings revealed significant decreasing in olfactory bulb volume and shallower olfactory sulcus in SZ patients. These structural changes are stable over time and are correlated with worst olfactory performances (Takahashi et al., 2013). Interestingly, Turetsky et al (2009) observed that those patients had normal orbital sulci. Shallower olfactory sulcus is often a result of an early embryogenesis disturbance. The orbital sulcus, which does not develop until the third trimester, is relatively immune to early insults. These differences reinforce the heuristic value of the neurodevelopmental hypothesis for SZ: at least for olfactory structures, disruption might begin in a defined temporal window – the first half of gestation. This revision highlights the potentialities of investigating OD in SZ as an useful insight for clinicians and researchers.