Author/Editor		Itoh, K; Mueller-Hoecker, J; Mehrain, P; Weis, S
Title		A morphometric study for cytochrome C oxidase of the substantia nigra in normal aging and Parkinson's disease
Type		članek
Source		Acta Stereol
Vol. and No.		Letnik 15, št. 2
Publication year		1996
Volume		str. 141-6
Language		eng
Abstract		Degeneration of the dopaminergic nigrostriatal system has been reported to occur with physiological aging as well as in Pakrinson's disease (PD). Defects of respiratory chain complexes were interpreted as a possible pathogenetic mechanism for cell death. In the present study, the substantia nigra of brains with normal aging and of brains from patients with PD was investigated by means of morphometry and immunohistochemisty. The antero-medial (Am), antero-intermediolateral (Ail), postero-medial (Pm), and postero-lateral (PI) nuclei of the substantia nigra were analysed using antibodies directed against the subunits II/III of cytochrome c oxidase (COX), the complex IV of the respiratory chain. In normal aging, the numerical density of melanin-positive neurons with COX defects was significantly increased in the four invstigated nuclei, namely Am, Ail, Pm, and Pl. The total number of neurons was only significantly decreased in the Pm nucleus. Intact neurons without COX defects were significantly reduced in the Pm and the Pl nuclei. The size of all types of neurons showed no significant differences with aging. In Parkinson's disease, the numerical density of pigmented neurons with COX defects were significantly incrased only in the Pl nucleus, whereas pigmented neurons without COX defects was significantly reduced in the nuclei Am, Ail and Pl. The cell size of pigmented neurons without COX defects was significantly reduced in the nuclei Am and Pl of PD cases. The data of the present study indicate that complex IV defects of neurons in the substantia nigra might be one cause of neuronal dysfunction occuring during physiologic aging. Furthermore, it is suggested that complex IV defects in nigral neurons are most probably due to accelerated aging rather than being a primary pathogenetic mechanism of PD.
Descriptors		PARKINSON DISEASE SUBSTANTIA NIGRA CYTOCHROME-C OXIDASE AGING NEURONS HISTOLOGICAL TECHNIQUES