title: Senile dementia: a threshold phenomenon of normal aging? A contribution to the functional reserve hypothesis of the brain.
abstract: Neurochemical investigations with normal aging brains show that in the first 70 years of life no major changes of the glycolytic pathway can be observed. Only in the following decades does a significant decrease of brain metabolic turnover occur. Changes in nerve cell size, one of the most relevant parameters in evaluating a diffuse nerve cell atrophy, appear in the brain cortex not earlier than between 85 and 94 years of age; a 21% nerve cell shrinkage is the mean. The results demonstrate that a significant decrease in turnover of the glycolytic pathway is followed by a significant but moderate shrinkage of the nerve cells after a delay of 10-15 years. Similar investigations in brains from senile demented subjects demonstrate that the change in glycolytic turnover is much more a quantitative than a qualitative phenomenon. In comparison with age-matched controls a decrease in glycolytic turnover of more than 60% is observed. Morphometric investigations of the nerve cell sizes in the brain cortex of senile demented subjects showed a decrease of 45-55% when compared with age-matched controls. When normal aging is compared with senile dementia it seems that old age dementia is a threshold phenomenon which starts if the glycolytic turnover drops below 50% of its value in young healthy adults. Physiological aging, however, stays within the range of the reserve capacity of normal brain performance. In conclusion, it seems that the exhaustion of the functional reserve capacity may shift an aging brain into a dementia syndrome.
authors.affiliation: Department of Pathology, University Medical School, Basel, Switzerland.
authors.forename: W
authors.initials: W
authors.lastname: Meier-Ruge
authors.forename: O
authors.initials: O
authors.lastname: Hunziker
authors.forename: P
authors.initials: P
authors.lastname: Iwangoff
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging; D001344:Autopsy; D001921:Brain / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D002256:Carbonic Anhydrases / Q000378:metabolism; D002540:Cerebral Cortex / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D003704:Dementia / Q000378:metabolism / Q000473:pathology*; D006019:Glycolysis; D006593:Hexokinase / Q000378:metabolism; D006801:Humans; D008875:Middle Aged; D011494:Protein Kinases / Q000378:metabolism; D012016:Reference Values
chemical_list: D011494:Protein Kinases; D006593:Hexokinase; D002256:Carbonic Anhydrases