Cerebral Blood Flow and Metabolism in Normal Human Aging, Pathological Aging, and Senile Dementia

Abstract

A review and a reappraisal are presented of earlier data on cerebral circulatory and metabolic studies in normal active elderly men (Group I) of mean age 71 years, compared with normal young subjects of mean age 21 years, conducted at the National Institutes of Health, Bethesda, MD, U.S.A., during 1956–1958. There was no significant difference in the mean CBF and cerebral metabolic rate for oxygen (CMRO2) values between the two populations; i.e., these important parameters did not fall with chronological aging per se. There was significant depression in the mean cerebral metabolic rate for glucose (CMRG) value (by ∼23%) in the aged compared with the young. Newer methods using positron emission tomography and appropriate isotopes have confirmed these findings in normal aging in human subjects and experimental animals. As expected, MABP and cerebral vascular resistance (CVR) were significantly elevated in the normal aged. MABP was even more elevated in elderly hypertensive subjects, and the CVR more elevated in the subjects with arteriosclerosis (Group II), who also showed a small but significant fall in CBF and in internal jugular venous Po2. The CBF showed a more pronounced fall in senile aged patients with chronic brain syndrome (Group III), in whom the CMRO2 also showed a marked drop (by ∼22%); the CMRG fell still further (∼40% of that in the young). Of the few aged subjects followed up after a lapse of 11 years by a repeat estimation of the same physiological and psychological parameters and of the EEG, most showed clear worsening, together with a fall in overall physical and intellectual performance, probably related to a rise in CVR and an increase in atherosclerosis with aging. Over this period, the number of surviving subjects fell strikingly from Group I to II to III. Our own limited observations and a brief review of the literature on “degenerative” and “vasogenic” dementias suggest that senile dementia, i.e., abnormal cerebral aging, results from the operation of both these factors or from one alone.