Given the functional anatomy of human olfactory pathways (e.g., Martzke et al., 1997; Seubert et al., 2013), olfactory deficits likely originate from brain structures in medial temporal lobe regions and orbitofrontal and dorsolateral prefrontal cortex linked to olfactory as well as cognitive and emotional disturbances in schizophrenia (e.g., Atanasova et al., 2008), and may help elucidate limbic system dysfunctions (Moberg et al., 2003). Thus, decreased olfactory threshold sensitivity in schizophrenia patients was associated with reduced volume in the perirhinal, but not entorhinal, region of the anterior ventromedial temporal lobe (Turetsky et al., 2003b), and both patients and their healthy relatives had reduced olfactory bulb volumes compared to healthy controls (Turetsky et al., 2003c). Also, Rupp et al. (2005) reported that poorer olfactory discrimination in schizophrenia patients was related to smaller hippocampal volumes, but not volumes in the orbitofrontal region. However, given that olfactory deficits have been observed across several neuropsychiatric and neurodegenerative disorders, including Parkinson’s and Alzheimer’s disease, it has been proposed that some aspects of impaired odor processing may share a common dopaminergic pathology, which may affect neurotransmission in
