Regression of Striatal Dendrites in Parkinson’s Disease

The clinical aspects of Parkinson’s disease (PD) were first characterized by James Parkinson in 1817 in his monograph “An Essay on Shaking Palsy”. He described the features of the illness as a proneness to tremor with a progressive decline in motor function marked by bradykinesia, rigidity and postural instability (Birkmayer and Riederer, 1983; Klawans and Tanner, 1984). The onset of the illness usually occurs in the sixth or seventh decade and thus, has been considered a disease of aging. Approximately 2 percent of the population over the age of 60 is afflicted with PD and prevalence is predicted to increase with prolonged longevity (Calne, 1970; Marttila, 1983). Neuropathological hallmarks include a loss of dopaminergic neurons in the pars compacta of the substantia nigra (SN) accompanied by a significant decline in the content of dopamine and activity of the synthetic enzyme, tyrosine hydroxylase (Hornykiewicz, 1982; Marsden, 1981). Less pronounced changes involve other neurotransmitter systems including a decline in choline acetyltransferase and glutamic acid decarboxylase activity in the striatum and norepinephrine and dopamine beta hydroxylase activity in the locus coeruleus (Hornykiewicz, 1982). Earlier studies have also reported cortical atrophy associated with an increase in the number of astrocytes, particularly in the frontal cortex, as well as general “senile changes” such as cortical cell loss, neurofibrillary degeneration and senile plaque formations (Turner, 1968).