Faculty Bibliography

Dexamethasone suppression tests (DSTs) were performed for 18 moderately demented elderly patients, 66 depressed elderly outpatients, and 25 age- and sex-matched healthy elderly control subjects. Seventeen percent of the demented patients and 4% of the normal subjects were DST nonsuppressors, compared to 38% of the total depressed group. The postdexamethasone plasma cortisol levels of the dementia group fell between those of the normal and the depressed subjects. In addition, demented patients had postdexamethasone cortisol levels significantly lower than those of depressed patients with high Hamilton depression scores. Older subjects in all diagnostic categories, including normal subjects, had higher postdexamethasone plasma cortisol levels

The development of FAST is of great importance to clinicians in identifying possibly remediable complications of Alzheimer's disease and distinguishing them from the characteristic progression of the illness. Premature loss of speech in an otherwise uncomplicated Alzheimer's-type presentation should lead the clinician to strongly suspect focal cerebral pathology, especially cerebral infarction

Elderly, community residing subjects (N = 106; mean age = 70.6 +/- 6.02 years) with cognitive functioning consistent with normal aging or dementia of the Alzheimer's type (DAT), were followed over a 3.6 year mean interval (range = 2.78 to 5.12 years). All subjects were assessed at baseline on the Global Deterioration Scale (GDS), a global clinical instrument reflecting the continuum of cognitive dysfunction from normal aging to severe DAT. At follow-up subjects were reassessed with respect to mortality, institutionalization and clinical change, defined as at least a two-point change on the 7-point GDS. Our results suggest that patients at deterioration levels GDS greater than or equal to 4, are more likely to show negative outcomes, specifically, institutionalization (Ps less than .001), death (Ps less than .01), or, for the community residing remainder, clinical deterioration (Ps less than .05), than subjects from less impaired (GDS = 2 or GDS = 3) subject groups. Seventy-six per cent of subjects at deterioration levels four or greater (N = 34) had negative outcomes at follow-up, whereas ninety percent of subjects with deterioration levels less than four (N = 72) did not.

Clinical conceptualizations with respect to cognition and dementia in late life have evolved rapidly in recent years. In contrast, many of the compounds that are currently widely prescribed for the amelioration of these conditions were introduced prior to the development of these concepts. Consequently, a reexamination of present and future criteria for drug trials, in accordance with current nosologic and clinical conceptualizations, is necessary at this time and is presented herein. This update will consist of four parts: (1) a brief historical examination of the evolution of current concepts, (2) a brief overview of the current diagnostic criteria that should be utilized in the identification of subjects for pharmacologic trials, (3) a brief overview of efficacy criteria, and (4) a brief overview of the status of pharmacologic investigations that have fulfilled the presently recommended standards

Six female outpatients with Alzheimer's disease (AD) along with four female controls of a similar age range were analyzed for sister chromatid exchangers (SCEs), cell cycle kinetics, and sensitivity to mutagens, in lymphocyte cultures. The mean level of SCEs for the AD patients was 11.40 SCEs/metaphase, while that for the controls was 9.12. The difference between the two groups was significant as shown by the Wilcoxon rank-sum test (p = 0.05). Cell cycle was 50% longer both in the AD patients (31.7 hr) and aged controls (31.5 hr) than in normal young adults (21.76 hr). Mitomycin-C (MMC) decreased the mitotic index in AD patients by 35% and in controls by only 12%. MMC also increased the cell cycle duration in AD patients by a greater extent (20%) than it did in the controls (13.5%), and AD cells were more sensitive to the toxic effects of bromodeoxyuridine. What appeared to be chromosomes with prematurely divided centromeres were also observed in AD cells