Feasibility of Mitochondrial Transplantation Via Nose‐To‐Brain Delivery for Treatment of Parkinson Diseases

Jui-Chih Chang*¹, Yi-Chun Chao¹, Huei-Shin Chang¹, Hui-Ju Chang¹, Wen-Ling Cheng¹, Ta-Tsung Lin¹ and Chin-San Liu*^1,2,3

Received: November 30, 2018;   Published: December 06, 2018

DOI: 10.26717/BJSTR.2018.11.002158

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Abstract

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