The pattern and course of cognitive impairment in late-life depression.

BACKGROUND: Cognitive deficits persist despite clinical recovery in subjects with late-life depression, but more needs to be known about their longer-term outcome and factors affecting their course. To investigate this, we followed the pattern of cognitive impairments over time and examined the effects of current mood, remission status, age of depression onset and antidepressant (AD) treatment on these deficits. METHOD: Sixty-seven subjects aged > or = 60 years with DSM-IV major depressive disorder and 36 healthy comparison subjects underwent tests of global cognition, memory, executive functioning and processing speed at baseline, 6 and 18 months, with some subjects tested again after 4 years. z scores were compared between groups, with analyses of clinical factors that may have influenced cognitive performance in depressed subjects. RESULTS: Half of the patients exhibited a generalized cognitive impairment (GCI) that persisted after 18 months. Patients performed worse across all cognitive domains at all time points, without substantial variability due to current mood, remission status or AD treatment. Late age of onset was associated significantly with decline in memory and executive functioning. Impaired processing speed may be a partial mediator of some deficits, but was insufficient to explain differences between patients and controls. Four-year follow-up data suggest impairments persist, but do not further decline. CONCLUSIONS: Cognitive deficits in late-life depression persist up to 4 years, affect multiple domains and are related to trait rather than state effects. Differences in severity and course between early and late onset depression suggest different pathogenic processes.

A questionnaire study for 128 patients with Gaucher disease.

Gaucher disease is an uncommon autosomal recessive disorder characterized by lysosomal storage of glucosyl ceramide, a material released during cell degradation. Patients with Gaucher disease often have significant hematologic, bone structural, and visceral problems which sometimes greatly affect their health and life style. Based on some extraordinary scientific discoveries over the past 45 years, a treatment system has evolved which consists of administration of an enzyme, which destroys the lysosome-stored material and to some extent restores the patients to good health. There are still some problems for these patients; however, and the purpose of the study is to define some of the clinical, sociologic, and psychologic problems with a specially designed questionnaire. Questionnaire data was collected for 128 patients from two institutions with complete anonymity, and the information compared against data from a National Health Interview Survey. The results show that many of the patients still have fairly extensive problems, which could possibly be helped by some alterations in treatment protocols.

A comparison of alveolar bone in young and aged mice.

To study the relationship between aging and alveolar bone loss, the periodontia of young (12-week-old) and aged (94-week-old) C57B1/6 Nia mice were compared, giving special attention to the alveolar bone. The tibiae were also examined to distinguish local from systemic bone changes. The mean area of interproximal bone between the first and second mandibular molars was significantly less in the aged mice than in the young mice. While there was no difference in the distance from the cementoenamel junction (CEJ) to the alveolar crest, the width of the interproximal bone was narrower in the aged animals. The cross-sectional width of the tibia was also reduced in the aged mice, although the total bony area remained constant. In both groups of animals, the distance from the apical extent of the inflammatory infiltrate to the alveolar crest was similar suggesting that alveolar bone loss was not related to inflammation. Other histologic features observed in the teeth of the aged mice, which may have influenced the amount of alveolar bone, were mesial tilting and distal drifting, occlusal wear, and passive eruption. These findings suggest that the greater bone loss in the aged mice may be more related to the aging process and to the functional changes of tooth movement associated with aging than to periodontal disease.