Preservation of midbrain catecholaminergic neurons in very old human subjects

Parkinson's disease is characterized by a progressive degeneration of dopam inergic neurons in the midbrain, yet the cause of this neuronal loss is sti ll unknown. It has been hypothesized that Parkinson's disease could be the consequence of accelerated ageing. In order to reveal a possible common pro cess during ageing and Parkinson's disease neurodegeneration, catecholamine rgic neurons of five anatomical regions of the brainstem (substantia nigra, central grey substance, ventral tegmental area, peri-and retrorubral area, and locus coeruleus) have been quantified using immunohistochemical staini ng for tyrosine hydroxylase (TH) on regularly spaced sections, between the rostral and caudal poles of the mesencephalon and in the rostral pole of th e pens, in post-mortem samples of 21 control subjects who died at ages 44-1 10 years. No statistically significant loss of TH positive neurons was obse rved in the older subjects, either in the substantia nigra or in the other midbrain regions that are known to degenerate to a lesser degree in Parkins on's disease. Furthermore, in the later regions no neuronal loss was observ ed from age 44 to 80 years, indicating that this result is not dependent on the inclusion of 'supernormal' very old people. These results suggest that from age 44 to 110 years, ageing in control adults is not, or is scarcely, accompanied by catecholaminergic cell loss in the midbrain and hence Parki nson's disease is probably not caused by an acceleration of a degenerative process during ageing.