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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

The authors examine the cross-sectional and longitudinal relation of smoking habits and current alcohol intake to cognitive status and decline over a 3-year period as well as the extent to which these relations are modified by the presence of clinical conditions indicating atherosclerosis (cardiovascular disease (CVD)/diabetes). Data are from the cohort of men followed in the longitudinal Zutphen Elderly Study in 1990 (n = 489) and 1993 (n = 333). Cognitive function was measured in 1990 and 1993 with the 30-point Mini-Mental State Examination (MMSE). After adjustment for age, education, and alcohol intake, current smokers made 20% more errors on the MMSE than never smokers in the cross-sectional analyses. Cognitive decline was greatest in those with CVD/diabetes who currently smoked and never smoked (-1.9 and -1.3 points, respectively). After adjustment for age, education, and smoking status, men with CVD/diabetes and low-to-moderate alcohol intake had a significantly lower risk for poor cognitive function (MMSE < or = 25) than abstainers (odds ratios of 0.3 for less than one drink and 0.2 for one to two drinks per day). Alcohol intake was not associated with cognitive decline. These findings do not support the hypothesis of a protective effect of smoking on cognitive function; they suggest that smoking may be harmful among those with CVD/diabetes. Alcohol may result in an acute beneficial effect on cognitive function among those with CVD/diabetes. However, selection bias and unmeasured confounding should be of concern when evaluating these results.
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PMID:Smoking, drinking, and thinking. The Zutphen Elderly Study. 856 Nov 55

Cognitive impairment is highly prevalent among the elderly. Subjects with disturbed glucose metabolism may be at risk of impaired cognitive function, as these disturbances can influence cognition through atherosclerosis, thrombosis and hypertension. We therefore studied the cross-sectional association of cognitive function with hyperinsulinaemia, impaired glucose tolerance and diabetes mellitus in a population-based cohort of 462 men aged 69 to 89 years. Cognitive function was measured by the 30-point Mini-Mental State Examination. Results were expressed as the rate ratio (95% confidence interval) of the number of erroneous answers given on the Mini-Mental State Examination by the index compared to the reference group. Compared to subjects with normal glucose tolerance, known diabetic patients had a rate ratio of 1.23 (1.04-1.46), newly-diagnosed diabetic patients of 1.16 (0.91-1.48) and subjects with impaired glucose tolerance of 1.18 (0.98-1.41), after adjustment for confounding due to age, occupation and cigarette smoking (p-trend = 0.01). Non-diabetic subjects in the highest compared to the lowest quartile of the area under the insulin curve had a rate ratio of 1.24 (1.03-1.50), after adjustment for confounding (p-trend = 0.02). The results did not change appreciably when potentially mediating factors, including cardiovascular diseases and risk factors associated with the insulin resistance syndrome, were taken into account. These results suggest that diabetes, as well as impaired glucose tolerance and hyperinsulinaemia in non-diabetic subjects are associated with cognitive impairment.
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PMID:Glucose intolerance, hyperinsulinaemia and cognitive function in a general population of elderly men. 859 25

Antioxidants have been implicated in processes related to atherosclerosis, aging, and selective neuronal damage, all of which may ultimately affect cognitive function. In a sample of older persons, the authors examined the cross-sectional relation between cognitive function and dietary intake of beta-carotene and vitamins C and E. The data were derived from 5,182 community participants aged 55-95 years in the population-based Rotterdam Study in the period 1990 to 1993. Dietary intake was estimated from a semi-quantitative food frequency questionnaire and categorized into five levels of intake. Cognitive function was measured with the 30-point Mini-Mental State Examination (MMSE) and characterized as unimpaired (> 25 points) or impaired (< or = 25 points). Logistic regression analysis was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for cognitive impairment. After adjustment for age, education, sex, smoking, total caloric intake, and intake of other antioxidants, a lower intake of beta-carotene was associated with impaired cognitive function (< 0.9 mg vs. > or = 2.1 mg intake, OR = 1.9, 95% CI 1.2-3.1; p for trend < 0.04). There was no association between cognitive function and intake of vitamins C and E. These cross-sectional observations are compatible with the view that beta-carotene-rich foods may protect against cognitive impairment in older people. The finding could also reflect unmeasured confounding, measurement error, or a change in food habits that resulted from rather than preceded the onset of cognitive impairment.
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PMID:Dietary antioxidants and cognitive function in a population-based sample of older persons. The Rotterdam Study. 868 96

The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 microns in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimer's disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimer's disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.
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PMID:Vascular pathology in three cases of progressive cognitive deterioration. 886 69

Dehydroepiandrosterone (DHEA; prasterone) is a major adrenal hormone with no well accepted function. In both animals and humans, low DHEA levels occur with the development of a number of the problems of aging: immunosenesence, increased mortality, increased incidence of several cancers, loss of sleep, decreased feelings of well-being, osteoporosis and atherosclerosis. DHEA replacement in aged mice significantly normalised immunosenescence, suggesting that this hormone plays a key role in aging and immune regulation in mice. Similarly, osteoclasts and lymphoid cells were stimulated by DHEA replacement, an effect that may delay osteoporosis. Recent studies do not support the original suggestion that low serum DHEA levels are associated with Alzheimer's disease and other forms of cognitive dysfunction in the elderly. As DHEA modulates energy metabolism, low levels should affect lipogenesis and gluconeogenesis, increasing the risk of diabetes mellitus and heart disease. Most of the effects of DHEA replacement have been extrapolated from epidemiological or animal model studies, and need to be tested in human trials. Studies that have been conducted in humans show essentially no toxicity of DHEA treatment at dosages that restore serum levels, with evidence of normalisation in some aging physiological systems. Thus, DHEA deficiency may expedite the development of some diseases that are common in the elderly.
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PMID:Dehydroepiandrosterone and diseases of aging. 889 25

Atherosclerosis and thrombosis may lead to cognitive impairment through cerebral infarcts or white matter hyperintensities. Oxidative stress is now seen as a major contributor to the process of atherogenesis. High intake of polyunsaturated fatty acids, e.g., linoleic acid, or low intake of antioxidants can increase oxidative stress. High intake of n-3 polyunsaturated fatty acids and its main source, fish, may reduce the risk of thrombosis. Little is known, however, about the relation between these dietary factors and cognitive function. The authors investigated this relation with data derived from a cohort of men, aged 69-89 years, who were participants in the Zutphen Elderly Study. The 30-point Mini-Mental State Examination was used to assess cognitive impairment in 1990 (score < or = 25 in 153/476 men, 32%) and cognitive decline from 1990 to 1993 (drop > 2 points in 51/342 men, 15%). Food intake was estimated in 1985 and 1990 by the cross-check dietary history method. High linoleic acid intake was associated with cognitive impairment after adjustment for age, education, cigarette smoking, alcohol consumption, and energy intake (odds ratio (OR) for highest vs. lowest tertile = 1.76, 95% confidence interval (CI) 1.04-3.01). Intake of n-3 polyunsaturated fatty acids was not associated with cognitive impairment, whereas high fish consumption tended to be inversely associated with cognitive impairment (OR = 0.63, 95% CI 0.33-1.21) and cognitive decline (OR = 0.45, 95% CI 0.17-1.16). Intakes of beta-carotene, vitamins C and E, and flavonoids were not inversely associated with cognitive impairment or decline. This study raises the possibility that high linoleic acid intake is positively associated with cognitive impairment and high fish consumption inversely associated with cognitive impairment.
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PMID:Polyunsaturated fatty acids, antioxidants, and cognitive function in very old men. 898 20

To clarify the neuropathologic criteria for the diagnosis of vascular dementia principally caused by large-vessel cerebral infarction, we solicited autopsy cases of vascular dementia from 10 university neuropathology laboratories. We included only those cases with progressive dementia clinically diagnosed as Alzheimer's disease (AD) or multi-infarct dementia, in whom autopsy revealed only cerebral infarction, without significant neuropathologic features of AD or other neurodegenerative disorders. Only six cases, all men, met these criteria. Each of them had, for a year or longer, gradually increasing cognitive impairment sufficient to interfere with daily activities, without clear evidence of "stepwise" progression. The age of onset of dementia was 66 years or less in five of the six patients. The duration of dementia ranged from 2 to 14 years. Five of the six cases had a history of either cerebral ischemia or acute stroke with residual focal neurologic deficits. Only two were known to have hypertension. At autopsy severe atherosclerosis of the cerebral arteries was present in three cases; two of these had a thrombotic occlusion of one internal carotid artery and one had partial obstruction of other cerebral arteries. In five of six brains, gross infarctions were present involving the thalamus, caudate, putamen, or large portions of the frontal, parietal, and temporal lobes of one or both hemispheres. Vascular amyloid was absent in all but one of these five brains. In four cases, the dementia was clinically indistinguishable from AD except for a history of focal neurologic deficits. The difficulty encountered in finding large numbers of cases of VaD without coexisting neuropathologic evidence of AD suggests that "pure" vascular dementia is very uncommon.
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PMID:Clinical-neuropathologic findings in multi-infarct dementia: a report of six autopsied cases. 940 94

Homocysteine (Hcy) may represent a metabolic link in the pathogenesis of atherosclerotic vascular diseases and old-age dementias. Hyperhomocysteinemia is an independent risk factor for coronary artery disease and peripheral vascular disease, and is also associated with cerebrovascular disease; specifically, the risk of extracranial carotid atherosclerosis significantly increases in relation to Hcy levels. Hcy is a reliable marker of vitamin B12 deficiency, a common condition in the elderly which is known to induce neurological deficits including cognitive impairment; a high prevalence of folate deficiency has been reported in psychogeriatric patients suffering from depression and dementia. Both these vitamins occupy a key position in the remethylation and synthesis of S-adenosylmethionine (SAMe), a major methyl donor in CNS; therefore, deficiencies in either of these vitamins lead to a decrease in SAMe and increase in Hcy, which can be critical in the aging brain. Another pathogenetic mechanism linking high Hcy levels to reduced cognitive performances in the elderly might be represented by excitotoxicity, since hyperhomocysteinemia may lead to an excessive production of homocysteic acid and cysteine sulphinic acid, which act as endogenous agonists of NMDA receptors. Considering the reasonably high prevalence in the general population of a genetic predisposition to a thermolabile form of the enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR), hyperhomocysteinemia can be seen as the result of multiple genetic and environmental factors leading to vascular and/or neurodegenerative disorders where age-related involutive phenomena represent a common pathogenetic ground. Systematic studies in different psychogeriatric conditions monitoring Hcy levels and clinical features before and after vitamin supplementation are therefore highly recommended.
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PMID:Role of homocysteine in age-related vascular and non-vascular diseases. 935 35

The results of longitudinal studies in geriatric medicine were reviewed by referring to relatively recent publications. "Longidufinal studies" comprised not only cohort studies but also prospective case-control studies in the broad sense. Poor self-rated health, weight loss hypoalbuminemia, inability to perform activities of daily living, low levels of physical activity, and cognitive dysfunction, all of which could be manifestations of chronic diseases, might shorten longevity. Cardiomegaly or left ventricular hypertrophy on ECG were again found to be important risk factors for cardiovascular disease in the aged, because of their relation to atherosclerosis. There is no evidence regarding the contribution of hyperlipidemia to the risk of cardiovascular disease in the aged, although insulin resistance can increase serum triglyceride levels and reduced level of high-density lipoprotein cholesterol even in the aged. Mortality due to stroke and heart disease have been decreasing in most developed countries, and several recent community-based studies have also shown decreases in the incidence of cerebral stroke. Large-scale case-control studies on the pharmacological treatment of hyperlipidemia have resulted in both primary and secondary prevention of coronary heart disease. However, information concerning the effects of treatment for hyperlipidemia on coronary heart disease in the aged is limited. Results of large-scale case-control studies indicate that pharmacological treatment of elderly hypertensive patients can reduce cardiovascular morbidity and mortality, and angiotensin-converting enzyme inhibitors have recently been shown ot be useful.
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PMID:[Longitudinal studies in geriatric medicine]. 971 Oct 88


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