Biopsies of olfactory epithelium in patients with Parkinson's disease

✍ Scribed by Martin Witt; Katja Bormann; Volker Gudziol; Kerstin Pehlke; Kathrin Barth; Amir Minovi; Antje Hähner; Heinz Reichmann; Thomas Hummel

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 462 KB
• Volume: 24
• Category: Article
• ISSN: 0885-3185
• DOI: 10.1002/mds.22464

✦ Synopsis

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder involving several neuronal systems. Impaired olfactory function may constitute one of the earliest symptoms of PD. However, it is still unclear to what degree changes of the olfactory epithelium may contribute to dysosmia and if these changes are different from those of other hyposmic or anosmic patients. This study aimed to investigate the hypothesis that olfactory loss in PD is a consequence of specific PD‐related damage of olfactory epithelium. Biopsies of 7 patients diagnosed with PD were taken. Six patients with PD were hyposmic, one anosmic. As non‐PD controls served 9 patients with hyposmia, 9 with anosmia, and 7 normosmic individuals. Further, nasal mucosa of 4 postmortem individuals was investigated. Immunohistochemical examinations were performed with antibodies against olfactory marker protein (OMP), protein gene product 9.5 (PGP 9.5), beta‐tubulin, (BT), proliferation‐associated antigen (Ki 67), the stem cell marker nestin, cytokeratin, p75NGFr, and α‐synuclein. Most of the biopsy specimens exhibited irregular areas of olfactory‐like, dysplastic epithelium positive for either PGP 9.5 or BT, but negative for OMP. No major histochemical differences in either the expression or distribution of these proteins were observed in the olfactory epithelium of patients with PD compared with controls. Reverse transcription PCR (RT‐PCR) data indicated mRNA for OMP in almost all subjects, independently of their olfactory performance. These data support the idea that olfactory loss in Parkinson's disease is not a consequence of damage to the olfactory epithelium but rather results from distinct central‐nervous abnormalities. © 2009 Movement Disorder Society