Nuclear magnetic resonance (NMR) imaging was employed to study 10 patients with Alzheimer's disease (AD) and seven healthy elderly control subjects. Coronal sections were used to make volumetric measurements of the hippocampus, ventricles, subarachnoid space, and brain parenchyma. The hippocampal volume (normalized relative to the size of the lenticular nucleus) was reduced by 40% in the AD group compared to the controls, with no overlap between the two groups. Overall measures of brain atrophy and ventricular and sulcal enlargement also showed significantly different group means, although with overlap between the two groups. Hippocampal atrophy did not correlate with either overall brain atrophy or dementia severity, although the degree of brain atrophy was correlated with dementia severity. These results show that NMR is capable of providing in vivo quantification of diminished hippocampal size in AD which is not correlated with overall brain atrophy and which may differentiate AD from normal aging.

Summary: Dynamic positron emission tomography with [ 18 Flfluorodeoxyglucose was used in six patients with Alzheimer's disease (AD) and seven healthy age-matched control subjects to estimate the kinetic parameters K 1*' k2 *, and k3 * that describe glucose transport and phospho rylation. A high-resolution tomograph was used to ac quire brain uptake data in one tomographic plane, and a radial artery catheter connected to a plastic scintillator was used to acquire arterial input data. A nonlinear iter ative least-squares fitting procedure that included terms for the vascular fraction and time delay to the peripheral sampling site was used to fit a three-compartment model to the brain data. Regions studied included frontal, tem poral, occipital, and the entire cortex and subcortical white matter. The values obtained for the individual rate constants and regional CMR g lc (rCMR g lc: calculated us ing regional values of the rate constants) were higher than those reported previously. A significant (p < 0.05) dePositron emission tomography (PET) has demon strated reduced regional CMRglc (rCMRg1J values in patients with Alzheimer ' s disease (AD). These findings predominate in temporal and parietal cor tical regions and have been reported by numerous laboratories (Benson et aI., 1983; Friedland et aI., 1983; Foster et aI., 1984; Duara et aI., 1986). De spite this agreement, however, the mechanisms and significance of these metabolic alterations are poorly understood.