*Corresponding author:
Jui-Chih Chang, Department of Vascular and Genomic Center, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 50094, TaiwanChin-san Liu, Department of Neurology, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 50094, Taiwan
Received: November 30, 2018; Published: December 06, 2018
DOI: 10.26717/BJSTR.2018.11.002158
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Olfactory dysfunction has been recently identified as one of the earliest non-motor symptoms of Parkinson’s disease (PD); it occurs at an early stage in approximately 90% of patients with PD and can be observed several years before the onset of limb disorders. Although the mechanism of olfactory dysfunction and its association with PD remain unclear, same symptoms have been observed in patients with Alzheimer disease and Down syndrome. Therefore, it is confirmed that the close association between the olfactory bulb (OB) and cranial nerves plays an important role in neurodegeneration [1]. The OB affects the function of dopaminergic neurons. Recent studies have demonstrated that the repeat unilateral intra-nasal administration (i.n.) of the mitochondrial inhibitor rotenone for 3-7 days can damage dopaminergic neurons in both sides of the OB, thereby resulting in olfactory dysfunction; the inhibitory effect is more pronounced in the i.n. side. Therefore, the result suggests that rotenone affects neuronal function via olfactory transport [2].
Abbreviations : PD: Parkinson’s Disease; OB: Olfactory Bulb; SN: Substantia Nigra; BBB: Blood–Brain Barrier; CNS: Central Nervous System; CSF: Cerebrospinal Fluid; BCSFB: Blood-CSF Barrier; DA: Dopamine; D0PAC: Di Hydroxy Phenyl Acetic Acid; CPP: Cell Penetrating Peptide
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