Pathophysiology of olfactory deficits in Parkinsons disease

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Oxidative stress-induced degeneration of do-paminergic neurons in the substantia nigra is an important pathological feature of PD. The presence of numerous dopaminergic neurons in the olfactory bulb might lead one to assume that olfactory dysfunction in PD is related to a loss of these neurons. In an effort to substantiate this assumption, anatomists in our research institute performed a quantitative analysis of the number of do-pamine neurons in the post-mortem human olfactory bulb. Quite contrary to the original expectations, a doubling of the number of TH-positive periglomerular neurons was found in the olfactory bulb of patients with a pathologically confirmed diagnosis of PD relative to age-matched controls (Huisman et al.,

2004). Considering that dopamine is known to inhibit neurotransmission between the axons of olfactory receptor cells and the dendrites of mitral cells within the glomeruli, it is tempting to speculate that the increase in dopaminergic neurons in the olfactory bulb is responsible for the hyposmia in PD. Along these lines, it would seem logical that olfactory dysfunction in PD does not improve with the administration of dopaminergic agents (Doty et al., 1988). Apparently, one of the earliest clinical signs of PD, i.e. impaired olfactory function, is unrelated to dopaminer-gic hypofunction.

Many questions raised by these observations remain to be answered. Firstly, one may wonder why dopaminergic neurons in the olfactory bulb are resistant to the degenerative process in PD. Perhaps their resistance is related to the absence of melanin, a possibility supported by the fact that several other populations of non-melanised dopaminergic neurons remain intact in PD. Secondly, it is unclear why there should be an increase in the number of dopaminergic neurons in the olfactory bulb. The tentative hypothesis that this may be a compensatory mechanism for the loss of nigral dopamine neurons is at odds with recent pathological observations that the olfactory bulb is affected by the disease process before the substantia nigra. Ultimately, we need to know in what way the known pathological changes, i.e. the increase in the number of dopaminergic neurons, the presence of Lewy bodies and neu-rites in the olfactory bulb and tract, and the neuronal loss in the anterior olfactory nucleus contribute to the olfactory deficits in PD.

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