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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the association of non-insulin-dependent (Type 2) diabetes mellitus and depression symptoms in a representative community-dwelling elderly population independently of other conditions such as gender, age, status, disability, cognitive impairment and a number of chronic medical conditions such as chronic obstructive lung disease, degenerative joint disease, heart disease, cirrhosis of the liver, cholelithiasis, peptic ulcer and kidney stones. A total of 1339 elderly subjects living in southern Italy were randomly selected from electoral rolls and evaluated. All subjects were tested by the Geriatric Depression Scale to detect depression, the Mini-Mental State Examination to study cognitive function and the Activity Daily Living Index to evaluate disability. Non-insulin-dependent diabetes mellitus affected 14.7% of our sample. Depression was more prevalent in women over 75 years of age than in younger women (15.9 vs 8.1%, p < 0.001). In multiple linear regression analysis, diabetes mellitus was found to be significantly associated with depression independently of age, gender, loneliness, cognitive impairment, chronic obstructive lung disease, degenerative joint disease, heart diseases, cancer, kidney disease, cirrhosis of the liver and cholelithiasis. It is concluded that non-insulin-dependent diabetes mellitus is significantly associated with depression in the elderly, which may have clinical implications for the achievement of sufficient blood glucose control.
Diabetes Metab 1996 Oct
PMID:Non-insulin-dependent diabetes mellitus is associated with a greater prevalence of depression in the elderly. The Osservatorio Geriatrico of Campania Region Group. 889 92

Type II (non-insulin-dependent) diabetes may be associated with impaired cognitive function. A detailed search of the literature has identified 19 controlled studies in which cognitive function in type II diabetes has been examined. The studies vary widely with respect to the nature of the diabetic populations studied and the psychological tests used. Thirteen studies demonstrated that the diabetic individuals performed more poorly in at least one aspect of cognitive function. The most commonly affected cognitive ability was verbal memory. Psychomotor ability and frontal lobe function were affected less consistently. The remaining six studies showed no differences in cognitive ability between subjects with type II diabetes and nondiabetic control subjects, but none had adequate statistical power to detect a between-group difference in cognitive ability of 0.5 of a standard deviation (a medium effect size). These findings are consistent with type II diabetes being associated with an increased risk of cognitive dysfunction. However, the widespread differences in methodology between the studies should lead to a cautious interpretation of their conclusions. The etiology of any cognitive decrement in type II diabetes is likely to result from an interaction between metabolic abnormalities intrinsic to diabetes, diabetes-specific complications, and other diabetes-related disorders.
Diabetes Care 1997 Mar
PMID:Is type II diabetes associated with an increased risk of cognitive dysfunction? A critical review of published studies. 905 2

Diabetes mellitus patients may develop changes in the brain that can lead to an impairment in cognitive performance. This paper reviews the results of research conducted with numerous neuropsychological assessment instruments. Cognitive impairment is particularly relevant among diabetic patients in the following domains, memory, attention, information processing, motor performance and executive functions. Several biomedical and psychosocial factors have been identified that increase the risk of developing cognitive impairment among this population duration and time of onset of the illness; the presence of several complications, such as peripheral neuropathy and recurrent severe hypoglycaemia; and premorbid intellectual functioning. The methodological difficulties involved in carrying out research in this field are discussed, as well as new research hypothesis.
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PMID:[Applications of neuropsychology in the medical field: diabetes mellitus as a model of research]. 905 3

We assessed the effect of diabetes and of episodes of severe hypoglycaemia on cognitive function in 28 diabetic children. Fifteen diabetic children (age 12.9 (SD 2.0) years) had experienced 1-4 episodes of severe hypoglycaemia. Five of these children diseased before the age of 5 years (SH-eod subgroup), and ten diseased after this age (SH-lod subgroup). Thirteen diabetic children (age 13.1 (SD 2.0) years) had not experienced episodes of severe hypoglycaemia (non-SH group). Each diabetic child was compared with a healthy control child of the same age and gender and with a similar social background. Neuropsychological assessment was blinded. The neuropsychological tests were grouped into one of seven cognitive domains. We found no effect on cognitive performance from diabetes per se or from severe hypoglycaemia in children with late-onset diabetes. However, early-onset diabetes was associated with low scores in two cognitive domains: psychomotor efficiency and attention. The SH-eod subgroup had lower scores than the SH-lod subgroup in psychomotor efficiency (p < 0.05) and also had lower scores than the SH-lod subgroup and the non-SH group in measures of attention (p < 0.05). Our results may indicate a slight cognitive dysfunction in children with early-onset diabetes who have experienced episodes of severe hypoglycaemia early in childhood.
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PMID:Cognitive function in type 1 diabetic children with and without episodes of severe hypoglycaemia. 905 83

The biochemical mechanisms by which diabetes modulates cognitive function are not well established. Here, we determined the effects of streptozotocin (STZ) administration on the binding properties of alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) subtypes of glutamate receptors in rats, using quantitative autoradiographic analysis of (3)H-AMPA and [(3)H]glutamate binding on brain tissue sections. The STZ injection (70 mg/kg intraperitoneally) produced a reduction of (3)H-AMPA binding in various brain regions, an effect that is due to a decrease in receptor affinity. The STZ-induced reduction of (3)H-AMPA binding varied in different brain structures, being more pronounced in the striatum, cerebral cortex, and hippocampus and almost absent in the cerebellum. Western blots performed on hippocampal membranes revealed that the decrease in (3)H-AMPA binding is possibly associated with changes in immunologic properties for one glutamate receptor subunit (GluR1). Finally, the effect of STZ-induced diabetes appeared to be specific to the AMPA subtype of glutamate receptors, as the same treatment did not modify [(3)H]glutamate binding to NMDA receptors. These changes in AMPA receptor properties may have important implications for understanding the biochemical mechanisms underlying cognitive impairment in diabetes.
Diabetes 1997 May
PMID:Binding properties of glutamate receptors in streptozotocin-induced diabetes in rats. 913 53

A follow-up study was conducted among men and women aged 55 years and over living in the community in order to estimate the incidence of initiation of antidepressant drug use and the association with chronic diseases. The study population consisted of 7,812 individuals. Overall, the incidence density for starting therapy with an antidepressant drug was 13.5 per 1000 person-years. The cumulative incidences after 1, 2 and 3 years were 1.3, 2.7 and 4.0%, respectively. The incidence in women was almost twice that in men and slightly higher in participants older than 70 years than in those younger than 70 years. The majority of the antidepressants prescribed were tricyclic antidepressants (65%), followed by selective serotonin reuptake inhibitors (23%) and other (12%) antidepressants. Only a minority (23%) received a dose considered effective for the indication of depression. Selective serotonin reuptake inhibitors were more often prescribed in an adequate dosage (68%) than were tricyclic antidepressants (12%) and other antidepressants (8%). Of the chronic diseases studied, only osteoarthritis and a history of stroke were predictors of initiation of antidepressant drug use after adjustment for age, sex and medical consumption. Hypertension, history of myocardial infarction, diabetes mellitus, rheumatoid arthritis, glaucoma, cognitive impairment and Parkinson's disease were not associated with future antidepressant drug use. No relevant differences were observed with respect to the choice of type of antidepressant drug among patients with chronic diseases. The present study indicates that each year antidepressant drug therapy is initiated in approximately 1.3% of the elderly. In general, the presence of chronic somatic diseases was not predictive of initiation of antidepressant drugs. Tricyclic antidepressants in this age group and in patients with certain chronic diseases may not be the optimal choice given their side-effects profile and drug-drug and drug-disease interactions. The predominance of these agents in the present study calls for further attention.
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PMID:Incidence of antidepressant drug use in older adults and association with chronic diseases: the Rotterdam Study. 934 83

It is now generally accepted that diabetes can alter central nervous system (CNS) function. Even in the absence of overt cerebrovascular accidents or repeated hypoglycemic reactions, uncontrolled hyperglycemia is associated with cognitive changes. These changes are documented both in patients with diabetes as well as in animal models of experimental diabetes. The cognitive impairment can be ameliorated with optimization of blood glucose control. The potential causes of CNS dysfunction in diabetes can be broadly categorized as either vascular causes including changes in the blood-brain barrier and metabolic changes. The latter causes include repeated hypoglycemic episodes, hyperglycemia, hyperosmolality, acidosis, ketosis, neuroendocrine or neurochemical changes. The other contributory causes of CNS dysfunction in diabetes include the presence of hypertension, uremia, peripheral and autonomic neuropathy and multiple drug use.
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PMID:Pathophysiology of central nervous system complications in diabetes mellitus. 935 75

Diabetics have impaired cognitive performance relative to age-matched control subjects, but the pathologic basis for this impairment is unknown. Because Alzheimer-type lesions, including both senile plaques and neurofibrillary tangles, contain glycated proteins and glycation is known to be increased in diabetes, we hypothesized that cognitive impairment in diabetes may be due in part to increased Alzheimer-type pathology. We measured the amount of Alzheimer-type pathology in postmortem brains of diabetic and age-matched control subjects with sensitive and specific histofluorescent and immunocytochemical methods. As expected, there were strong correlations between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between the pathologic measures. On the other hand, there was no significant difference between diabetics and control subjects with respect to severity of Alzheimer-type pathology, on average, or with respect to age. This finding was true for diabetics with and without insulin dependence. The results confirm reports showing that diabetes is not a risk factor for Alzheimer-type pathology and suggest that factors other than Alzheimer's disease are responsible for cognitive impairment in diabetics.
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PMID:Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects. A retrospective postmortem immunocytochemical and histofluorescent study. 937 13

This study assessed clinical and demographic differences between 74 geriatric psychiatry outpatients with early-onset vs late-onset depression. The following data were considered: age, gender, marital status, years of education, number of prescription medications and active medical diagnoses (including presence of various categories of medical disorder), presence of any comorbid dementia or other psychiatric disorder, age of depression onset, number of depressive episodes and MMSE score. Fifteen patients (20.3%) had an early onset of depression (before age 60 years) and 59 (79.7%) had a late onset of depression. Early-onset patients had significantly more episodes of depression than late-onset patients (4.2 vs 1.9, t = 4.74, p < 0.001). Patients with early-onset depression also had a higher mean number of prescribed medications (5.3 vs 3.5, t = 2.29, p = 0.025) and active medical disorders (4.6 vs 3.1, t = 2.89, p = 0.005). Specifically, early onset of depression was associated with an elevated prevalence of cardiac disease (53.3% vs 23.7%, chi 2 = 5.0, df = 1, p = 0.025), diabetes (46.7% vs 16.9%, chi 2 = 6.0, df = 1, p = 0.015), gastrointestinal disorder (40.0% vs 12.0%, chi 2 = 6.5, df = 1, p = 0.011) and arthritis (26.7% vs 6.8%, chi 2 = 4.9, df = 1, p = 0.027). These findings support previous reports that people with a history of depression experience greater medical morbidity than those without a history of depression. The study groups did not differ with respect to MMSE score or presence of a concurrent dementia disorder. These results were unexpected given previous studies that indicate greater cognitive impairment in late- vs early-onset depression. The potential contribution of increased vascular risk factors among the early-onset depression group may have partly contributed to the finding of no difference in cognition between groups in the present study.
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PMID:Differences in geriatric psychiatry outpatients with early- vs late-onset depression. 942 94

Recent findings of a linkage between high blood pressure (BP) and later development of dementia have given new prospects on cerebral target-organ damage in hypertension and have added substance to the concept of "preventable senility." The aim of this study was to analyze the impact of hypertension, circadian BP profile, and disturbed glucose metabolism on cognitive function. The study population consisted of 999 seventy-year-old men from a population-based cohort study in Uppsala, Sweden, followed with respect to cardiovascular risk factors since the age of 50 years. At the age of 70, 24-hour ambulatory BP was monitored together with measurements of insulin sensitivity, glucose tolerance, serum lipids, and lipoproteins. Cognitive function was assessed by the Mini-Mental State Examination and the Trail-Making Test. High diastolic BP at baseline predicted later impaired cognitive performance, even after excluding men with a previous stroke (n = 70). Cross-sectional measurements at age 70 showed that high 24-hour BP, nondipping, insulin resistance, and diabetes all were related to low cognitive function. The relationships between hypertension and cognitive impairment were strongest in untreated men. These data from a general population of healthy elderly men indicate that hypertension and associated metabolic disturbances might be susceptibility factors for cognitive disorders. The findings add support to possibilities of intervention in early stages in cognitive decline, ie, before manifest dementia.
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PMID:Hypertension is related to cognitive impairment: a 20-year follow-up of 999 men. 949 61


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