Gender‐related changes in increase of dopaminergic neurons in the olfactory bulb of Parkinson's disease patients

Huisman, Evelien; Uylings, H.B.M.; Hoogland, Piet V.

doi:10.1002/mds.22009

Cited by 94 publications

(61 citation statements)

References 42 publications

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“…Our results suggest that olfactory dysfunction in PD is associated with atrophy in olfactory-eloquent regions of the limbic and paralimbic cortex and might therefore not be restricted to deficient sensory transmission in the olfactory bulb (Huisman et al, 2008). Further analysis showed that olfactory-related atrophy is not a consequence of generalized brain atrophy but seems to be rather a regional effect; total intracranial and gray matter volumes did not differ between all groups.…”

Section: Discussionmentioning

confidence: 51%

“…A prevalent symptom at early stages of PD is olfactory impairment (Ansari and Johnson, 1975). Results from postmortem studies revealed pathological changes (Lewy body formation) in the olfactory bulb (Huisman et al, 2008) but also in other brain regions related to olfaction, such as the anterior olfactory nucleus (Pearce et al, 1995), the piriform cortex (Braak et al, 2003;Silveira-Moriyama et al, 2009), the amygdaloid complex (Harding et al, 2002;Braak et al, 2003), the entorhinal cortex, and the hippocampal formation (Braak et al, 2003). Using functional magnetic resonance imaging in PD patients, our previous findings indicated altered neuronal activity in the amygdaloid complex and hippocampal formation during olfactory stimulation (Westermann et al, 2008;Welge-Lüssen et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Olfactory Impairment Predicts Brain Atrophy in Parkinson's Disease: Figure 1.

Wattendorf¹,

Welge‐Lüssen²,

Fiedler³

et al. 2009

J. Neurosci.

141

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Olfactory dysfunction is a frequent nonmotor symptom in idiopathic Parkinson's disease (PD) and may be considered as an early clinical feature of the disease preceding motor symptoms by years. According to recent neuropathological staging concepts, impaired olfaction is assumed to indicate an early pathological process and might be associated with structural changes in the brain. A morphometric analysis of magnetic resonance images [voxel-based morphometry (VBM)] was used to investigate gray matter atrophy related to psychophysically measured scores of olfactory function in early PD patients (n ϭ 15, median Hoehn and Yahr stage 1.5), moderately advanced PD patients (n ϭ 12, median Hoehn and Yahr stage 2.5), and age-matched healthy controls (n ϭ 17). In PD patients, but not in controls, cortical atrophy in olfactory-related brain regions correlated specifically with olfactory dysfunction. Positive correlations between olfactory performance and gray matter volume were observed in the right piriform cortex in early PD patients and in the right amygdala in moderately advanced patients. The results provided first evidence that olfactory dysfunction in PD is related to atrophy in olfactory-eloquent regions of the limbic and paralimbic cortex. In addition, olfactory-correlated atrophy in these brain regions is consistent with the assumption that olfactory impairment as an early symptom of PD is likely to be associated with extranigral pathology.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Olfactory Impairment Predicts Brain Atrophy in Parkinson's Disease: Figure 1.

Wattendorf¹,

Welge‐Lüssen²,

Fiedler³

et al. 2009

J. Neurosci.

141

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“…These neurons are calciumdependent autonomous pacemakers (91). However, there are no signs of cell loss in the olfactory bulb in spite of deficits in olfaction being a harbinger of the motor symptoms in PD (50,94). This does not mean that a reliance upon calcium is a bad thing though, as this region is capable of adult neurogenesis (90).…”

Section: Pd Is Not Just a Disease Of Dopaminergic Neurons In The Sncmentioning

confidence: 99%

The Origins of Oxidant Stress in Parkinson's Disease and Therapeutic Strategies

Surmeier

Guzmán

Sánchez-Padilla

et al. 2011

Antioxidants & Redox Signaling

135

109

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Parkinson's disease (PD) is a major world-wide health problem afflicting millions of the aged population. Factors that act on most or all cell types (pan-cellular factors), particularly genetic mutations and environmental toxins, have dominated public discussions of disease etiology. Although there is compelling evidence supporting an association between disease risk and these factors, the pattern of neuronal pathology and cell loss is difficult to explain without cell-specific factors. This article focuses on recent studies showing that the neurons at greatest risk in PD-substantia nigra pars compacta dopamine neurons-have a distinctive physiological phenotype that could contribute to their vulnerability. The opening of L-type calcium channels during autonomous pacemaking results in sustained calcium entry into the cytoplasm of substantia nigra pars compacta dopamine neurons, resulting in elevated mitochondrial oxidant stress and susceptibility to toxins used to create animal models of PD. This cellspecific stress could increase the negative consequences of pan-cellular factors that broadly challenge either mitochondrial or proteostatic competence. The availability of well-tolerated, orally deliverable antagonists for L-type calcium channels points to a novel neuroprotective strategy that could complement current attempts to boost mitochondrial function in the early stages of the disease.

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“…12 The existence and targeting of neuronal loss in the olfactory system is controversial. 48,49 This issue is complicated by the neurogenesis in this region. 50 There are several other regions that have been reported to have either neuronal loss or Lewy pathology in PD, many in single studies.…”

Section: Introductionmentioning

confidence: 99%