Abstract
In the human brain angiotensin converting enzyme (ACE, EC 3.4.15.1) exists in two forms of activity [il. ACE is mainly found in a membrane-fund fraction of cortical epithelial cells, catalysing the conversion of inactive an~otensin I to hypertensive angiotensin II [2}. A soluble ACE form is located neuronally within the corpus striatum and may hydrolyse neuropeptides with a messenger function [3]. ACE activity in normal human lumbar cerebrospinal fluid (CSF), may largely reflect ACE activity in non-cortical regions of the brain, for instance the basal ganglia [4]. It is therefore of interest to evaluate the activity of ACE in neurological disease, such as Parkinson’s disease (PD), with a degeneration of the nigrostriatal dopaminergic neurons and consequent striatal dopamine depletion. Previous studies in PD patients have shown either decreased [5] or normal [6] CSF ACE activity. These authors, however, have not studied untreated and treated PD patients separately. Recently, increased CSF ACE activity in schizophrenic patients
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