[Cerebral glucose metabolism in presenile dementia of the Alzheimer type--follow-up of therapy with muscarinergic choline agonists].

In 8 patients who had clinically diagnosed presenile dementia (Alzheimer's disease) the cerebral glucose metabolism was repeatedly determined via FDG-PET under therapy with a muscarinergic choline agonist. The pattern of glucose metabolism disturbance characteristic of Alzheimer's disease, which had been determined previously by examining the metabolism, was confirmed. Whereas the total cortical glucose metabolism was significantly reduced, the regions of the parietal and the adjacent regions of the temporal and occipital association cortex were preferably affected. The primary somatosensory and visual cortex were largely excepted from the reduction in metabolism or showed slightly enhanced metabolic rates, as for example the cerebellum. The disturbance was not equilaterally pronounced and correlated with the neuropsychological deficiency. Despite biochemically "on target" therapy the glucose metabolism decreased progressively (mean value with large interindividual and intraindividual variations. No relationship between the degree of reduced metabolism and the clinical pattern was seen. Rather, it appears that the clinical pattern is much more strongly influenced by mutual adjustment of metabolic differences in various areas of the brain. Results obtained by the authors are communicated besides a review of update knowledge and interpretation of pathophysiological and biochemical linkups in Alzheimer's disease, taking into consideration the glucose metabolism studies published in the literature.