Subclinical dopaminergic dysfunction in asymptomatic Parkinson's disease patients' relatives with a decreased sense of smell
Article first published online: 27 APR 2001
Copyright © 2001 Wiley-Liss, Inc.
Annals of Neurology
Volume 50, Issue 1, pages 34–41, July 2001
How to Cite
Berendse, H. W., Booij, J., Francot, C. M. J. E., Bergmans, P. L. M., Hijman, R., Stoof, J. C. and Wolters, E. Ch. (2001), Subclinical dopaminergic dysfunction in asymptomatic Parkinson's disease patients' relatives with a decreased sense of smell. Ann Neurol., 50: 34–41. doi: 10.1002/ana.1049
- Issue published online: 26 JUN 2001
- Article first published online: 27 APR 2001
- Manuscript Revised: 29 JAN 2001
- Manuscript Accepted: 29 JAN 2001
- Manuscript Received: 19 JUN 2000
- ZorgOnderzoek Nederland
By the time a clinical diagnosis of Parkinson's disease (PD) is made, a significant loss of dopaminergic neurons has already occurred. Identifying patients in the period between the presumed onset of dopaminergic cell loss and the appearance of clinical parkinsonism may be of major importance in the development of effective neuroprotective treatment strategies. In an effort to develop a feasible strategy to detect preclinical PD, a combination of olfactory processing tasks, including odor detection, odor identification, and odor discrimination was used to select groups of hyposmic and normosmic individuals from a total of 250 relatives (parents, siblings, or children) of subjects with PD. Single photon emission computed tomography (SPECT) with [123I]β-CIT as a dopamine transporter ligand was used to assess nigrostriatal dopaminergic function in 25 hyposmic and 23 normosmic relatives of PD patients. An abnormal reduction in striatal dopamine transporter binding was found in 4 out of 25 hyposmic relatives of PD patients, 2 of whom subsequently developed clinical parkinsonism, and in none of the 23 normosmic relatives. These observations demonstrate that subclinical reductions in dopamine transporter binding can be detected in asymptomatic relatives of sporadic PD patients by means of [123I]β-CIT and SPECT. The results further indicate that olfactory deficits may precede clinical motor signs in PD.