Gene/Protein Disease Symptom Drug Enzyme Compound
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 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reducing food intake in lower animals such as the rat decreases body weight, retards many aging processes, delays the onset of most diseases of old age, and prolongs life. A number of clinical trials of food restriction in healthy adult human subjects running over 2-15 years show significant reductions in body weight, blood cholesterol, blood glucose, and blood pressure, which are risk factors for the development of cardiovascular disease and diabetes. Lifestyle interventions that lower energy balance by reducing body weight such as physical exercise can also delay the development of diabetes and cardiovascular disease. In general, clinical trials are suggesting that diets high in calories or fat along with overweight are associated with increased risk for cardiovascular disease, type 2 diabetes, some cancers, and dementia. There is a growing literature indicating that specific dietary constituents are able to influence the development of age-related diseases, including certain fats (trans fatty acids, saturated, and polyunsaturated fats) and cholesterol for cardiovascular disease, glycemic index and fiber for diabetes, fruits and vegetables for cardiovascular disease, and calcium and vitamin D for osteoporosis and bone fracture. In addition, there are dietary compounds from different functional foods, herbs, and neutraceuticals such as ginseng, nuts, grains, and polyphenols that may affect the development of age-related diseases. Long-term prospective clinical trials will be needed to confirm these diet-disease relationships. On the basis of current research, the best diet to delay age-related disease onset is one low in calories and saturated fat and high in wholegrain cereals, legumes, fruits and vegetables, and which maintains a lean body weight. Such a diet should become a key component of healthy aging, delaying age-related diseases and perhaps intervening in the aging process itself. Furthermore, there are studies suggesting that nutrition in childhood and even in the fetus may influence the later development of aging diseases and lifespan.
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PMID:Dietary approaches that delay age-related diseases. 1804 54

Vascular risk factors, such as type 2 diabetes, hypertension, obesity and dyslipidaemia often co-occur. Each of these factors has been associated with an increased risk of dementia, but it is uncertain which factor imposes the greatest risk. Moreover, the effect of age at time of exposure may differ across factors. This paper systematically reviews the evidence for the association of each of these risk factors with dementia. Longitudinal population-based studies that assessed the incidence of dementia in relation to diabetes (n=14), hypertension (n=13), dyslipidaemia (n=8) or obesity (n=9) were included. All four risk factors were indeed associated with an increased risk of dementia, but the results of studies on diabetes and obesity were most consistent. The magnitude of the effects was comparable across the risk factors, with odds ratios for 'any dementia' around 1.5. For hypertension, obesity and dyslipidaemia age appeared to modulate the association: the risk of dementia was generally largest in studies that measured the risk factor in midlife (compared to late life) and had a long follow-up time. At midlife, the population attributable risk of dementia was highest for hypertension, up to 30% of cases of late life dementia. Later in life diabetes appears to convey the highest risk of dementia. This review shows that vascular risk factors should be regarded as a major target for preventive measures, but that timing of such measures appears to be critical.
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PMID:Diabetes and other vascular risk factors for dementia: which factor matters most? A systematic review. 1839 1

Alzheimer's disease, AD, is the most common form of dementia. AD initially targets memory and progressively destroys the mind. The brain atrophies as the neocortex suffers neuronal, synaptic, and dendritic losses, and the hallmark amyloid plaques and neurofibrillary tangles proliferate. Pharmacological management, at best, is palliative and transiently effective, with marked adverse effects. Certain nutrients intrinsic to human biochemistry (orthomolecules) match or exceed pharmacological drug benefits in double-blind, randomized, controlled trials, with superior safety. Early intervention is feasible because its heritability is typically minimal and pathological deterioration is detectable years prior to diagnosis. The syndrome amnestic mild cognitive impairment exhibits AD pathology and to date has frustrated attempts at intervention. The condition age-associated memory impairment is a nonpathological extreme of normal brain aging, but with less severe cognitive impairment than amnestic mild cognitive impairment. Age-associated memory impairment is a feasible target for early intervention against AD, beginning with the modifiable AD risk factors - smoking, hypertension, homocysteine, type 2 diabetes, insulin resistance, and obesity. Stress reduction, avoidance of toxins, and mental and physical exercise are important aspects of prevention. The diet should emphasize omega-3 fatty acids docosahexaenoic acid and eicosapentaenoic acid; flavonoids and other antioxidant nutrients; and B vitamins, especially folate, B6 and B12. Dietary supplementation is best focused on those proven from randomized, controlled trials: the phospholipids phosphatidylserine and glycerophosphocholine, the energy nutrient acetyl-L-carnitine, vitamins C and E, and other antioxidants. A comprehensive integrative strategy initiated early in cognitive decline is the most pragmatic approach to controlling progression to Alzheimer's disease.
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PMID:Alzheimer's disease, amnestic mild cognitive impairment, and age-associated memory impairment: current understanding and progress toward integrative prevention. 1859 Mar 47

We aimed to develop a prediction rule for urinary tract infections (UTIs) in patients with type 2 diabetes mellitus (DM2). A 12-month prospective cohort study was conducted in patients with DM2 aged > or = 45 years to predict the occurrence of recurrent UTIs in women and lower UTIs in men. Predictors for recurrent UTI in women (n=81, 2%) and lower UTIs in men (n=93, 3%) were age, number of general practitioner (GP) visits, urinary incontinence, cerebrovascular disease or dementia. In women, renal disease was an additional predictor. The optimism [corrected] corrected area under the receiver-operating curve (AUC) was 0.79 (95% CI 0.74-0.83) for women and 0.75 (95% CI 0.70-0.80) for men. Using a cut-off score of 4, women with a lower risk assignment had a probability of 0.3% for the outcome. For a cut-off score of 6, women with a higher risk assignment had a probability of 5.8%. For men these figures were 0.8 and 7.1 for a cut-off score of 2 and 4, respectively. Simple variables can be used for the risk stratification of patients.
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PMID:A clinical prediction rule for urinary tract infections in patients with type 2 diabetes mellitus in primary care. 1863 26

The Pro12Ala polymorphism in the PPAR-gamma gene has been associated with reduced incidence of type 2 diabetes. Although diabetes has been implicated as a risk factor for dementia, the association of Pro12Ala with cognitive impairment is unclear. Dementia and cognitive impairment without dementia (CIND) were determined during six annual follow-up evaluations in a cohort of 929 older Latinos. Among those with diabetes at baseline, there was an increased rate of dementia/CIND for Ala carriers compared to non-carriers (adjusted hazard ratio (HR)=2.5, 95% confidence interval (CI): 1.3-4.9) but not among non-diabetic participants (adjusted HR=0.94; 95% CI: 0.49-1.8). Among males, there was also an increased rate for Ala carriers (adjusted HR=2.7, 95% CI: 1.4-5.2) but not among female carriers (adjusted HR=0.88; 95% CI: 0.47-1.6). The rate of dementia/CIND was highest in diabetic male Ala carriers (adjusted HR=4.2; 95% CI: 1.5-11) compared to non-diabetic male carriers (adjusted HR=2.9; 95% CI: 1.1-7.4), diabetic female carriers (HR=1.6; 95% CI: 0.66-4.1), and non-diabetic female carriers (HR=0.52; 95% CI: 0.21-1.3). These data suggest that although the Ala variant is associated with a reduced risk of type 2 diabetes, it may increase the risk of cognitive impairment in individuals once diabetes has developed. Male Ala carriers may also have a greater risk of dementia/CIND.
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PMID:The PPAR-gamma Pro12Ala polymorphism and risk of cognitive impairment in a longitudinal study. 1863 67

Despite mortality due to communicable diseases, poverty, and human conflicts, dementia incidence is destined to increase in the developing world in tandem with the ageing population. Current data from developing countries suggest that age-adjusted dementia prevalence estimates in 65 year olds are high (>or=5%) in certain Asian and Latin American countries, but consistently low (1-3%) in India and sub-Saharan Africa; Alzheimer's disease accounts for 60% whereas vascular dementia accounts for approximately 30% of the prevalence. Early-onset familial forms of dementia with single-gene defects occur in Latin America, Asia, and Africa. Illiteracy remains a risk factor for dementia. The APOE epsilon4 allele does not influence dementia progression in sub-Saharan Africans. Vascular factors, such as hypertension and type 2 diabetes, are likely to increase the burden of dementia. Use of traditional diets and medicinal plant extracts might aid prevention and treatment. Dementia costs in developing countries are estimated to be US$73 billion yearly, but care demands social protection, which seems scarce in these regions.
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PMID:Alzheimer's disease and vascular dementia in developing countries: prevalence, management, and risk factors. 1870 94

The occurrence of diabetes and dementia is very high in older patients. The fact that both conditions are concurrent raises the question of a possible link between the two. Cognitive functions of non-demented patients with diabetes have been extensively studied. In type 1 diabetes, only a mild decrease of the speed of information processing and of the psychomotor efficiency has been shown. Cognitive decline seems to be related to poor metabolic control and not to hypoglycaemia. In older patients with type 2 diabetes, memory and executive functions have been found impaired. Longitudinal studies of the literature have shown that diabetic patients have a higher chance of developing dementia than non-diabetic patient, with a relative risk (RR) between 1.26 and 2.83. The risk of vascular dementia was increased in 3 out of 5 studies, with a RR ranging between 2 and 2.6. With regard to Alzheimer's disease, the results are conflicting. Half of the studies found an increased risk in diabetic patients (RR: 1.3-2). The possible causal mechanisms of dementia in diabetic patients remain hypothetical. MRI studies showed varying degrees of cortical atrophy, cerebral infarcts and deep white matter lesions. In neuropathological studies, senile plaques and neurofibrillary tangle were not found with higher severity in the brain of diabetic patients than in the brain of age-matched controls. Several hypotheses have been raised to explain the relationship between diabetes and cognitive decline. Micro and macrovascular changes in the brain could induce cerebral hypoxia and ischemic conditions resulting in cellular death or white matter lesions. The occurrence of vascular lesions might reduce the threshold at which dementia will occur in Alzheimer disease. The deposition of advanced glycation end products doesn't spare the brain and they have been found in senile plaques, where they can reduce the solubility of proteins such as the beta amyloid and Tau proteins. Some authors favour the hypothesis of a brain insulin resistance because, in a few small studies, insulin was found to improve memory.
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PMID:[Diabetes mellitus and cognition: is there a link?]. 1878 78

Type 2 diabetes is a major health problem associated with excess mortality and morbidity. Vascular complications are one of the most serious consequences of this disorder. Moreover, type 2 diabetes is also a risk factor for cerebral complications, including cognitive impairment and dementia. However, it has been shown that tight glycemic control contributes to reduce the incidence of diabetes-associated complications. Metformin is a potent antihyperglycemic agent widely used in the management of type 2 diabetes whose main actions are the suppression of gluconeogenesis and the improvement of glucose uptake and insulin sensitivity. This review is mainly devoted to describe the mechanisms of action underlying the antidiabetic effects of metformin. Furthermore, we will present evidence for the protective effects of metformin against diabetes-associated complications mainly cerebral and vascular complications. Finally, we will describe the few known side effects associated to this antidiabetic agent.
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PMID:Mechanisms of action of metformin in type 2 diabetes and associated complications: an overview. 1899 52

Using a method based on ESR spectroscopy and spin-trapping, we have shown that Abeta (amyloid beta-peptide) (implicated in Alzheimer's disease), alpha-synuclein (implicated in Parkinson's disease), ABri (British dementia peptide) (responsible for familial British dementia), certain toxic fragments of the prion protein (implicated in the transmissible spongiform encephalopathies) and the amylin peptide (found in the pancreas in Type 2 diabetes mellitus) all have the common ability to generate H(2)O(2) in vitro. Numerous controls (reverse, scrambled and non-toxic peptides) lacked this property. We have also noted a positive correlation between the ability of the various proteins tested to generate H(2)O(2) and their toxic effects on cultured cells. In the case of Abeta and ABri, we have shown that H(2)O(2) is generated as a short burst during the early stages of aggregation and is associated with the presence of protofibrils or oligomers, rather than mature fibrils. H(2)O(2) is readily converted into the aggressive hydroxyl radical by Fenton chemistry, and this extremely reactive radical could be responsible for much of the oxidative damage seen in all of the above disorders. We suggest that the formation of a redox-active complex involving the relevant amyloidogenic protein and certain transition-metal ions could play an important role in the pathogenesis of several different protein misfolding disorders.
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PMID:Metal-dependent generation of reactive oxygen species from amyloid proteins implicated in neurodegenerative disease. 1902 43

As the number of elderly persons in our country increases, more attention is being given to geriatric healthcare needs and successful ageing is becoming an important topic in medical literature. Concept of successful ageing is in first line on a preventive approach of care for older people. Promotion of regular physical activity is one of the main non-pharmaceutical measures proposed to older subjects as low rate of physical activity is frequently noticed in this age group. Moderate but regular physical activity is associated with a reduction in total mortality among older people, a positive effect on primary prevention of coronary heart disease and a significant benefit on the lipid profile. Improving body composition with a reduction in fat mass, reducing blood pressure and prevention of stroke, as well as type 2 diabetes, are also well established. Prevention of some cancers (especially that of breast and colon), increasing bone density and prevention of falls are also reported. Moreover, some longitudinal studies suggest that physical activity is linked to a reduced risk of developing dementia and Alzheimer's disease in particular.
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PMID:Health benefits of physical activity in older patients: a review. 1919 69


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