Idiopathic Parkinson's disease (PD) is closely associated with olfactory loss. Deficits in the sense of smell may precede clinical motor symptoms by years. Although there is more and more evidence from recent studies to support this view, it remains unclear which substrates would cause the olfactory deficit. Studies based on biopsies from the olfactory epithelium did not reveal specific changes in the nasal mucosa of PD patients compared to patients who were hyposmic for other reasons. Thus, PD-related olfactory impairment seems not to be directly associated with specific changes in the olfactory epithelium. With regard to volumetrics of the olfactory bulb (OB) results indicated that there is little or no difference between PD patients and healthy controls in terms of OB volume. Again, these data support the idea that olfactory loss in PD is not a consequence of damage to the olfactory epithelium but rather results from central-nervous changes. Finally, studies based on functional MRI suggested that neuronal activity in the amygdala and hippocampus is reduced in PD patients compared to controls which may specifically impact on olfactory function. In addition, neuronal activity in components of cortico-striatal loops appears to be up-regulated indicating compensatory processes involving the dopaminergic system. Thus, it seems that cerebral changes, and not changes at the level of the olfactory epithelium, are the basis of the olfactory loss observed in PD patients.