1,721,125 research outputs found
Vascular genetic factors and lipoprotein metabolism in human longevity
No full textComplex inter-relationships between age-associated illnesses such as vascular disease and Alzheimer’s disease (AD) suggest that biological and genetic pathways may be worthy of examination in centenarian populations to provide insights into human longevity. The search for factors involved in aging and longevity has progressed extensively in the recent years because of increased human life expectancy and elevation of the number of elderly people. Different genetic and non genetic factors have been examined in the quest to understand the biological basis of human longevity. Indeed, it can be hypothesised that centenarians have environmental and genetic factors that confer unexpected survival advantage. Examples of such advantage are characterized by marked delay or escape from age-related diseases, such as coronary artery disease (CAD), cerebrovascular disease (CVD), and AD, respectively, the first, the third, and the fourth largest causes of mortality, in the western populatio n. Th us one can suggest that genes and biochemical factors likely to be implicated in these disorders may have a role in human longevity. In this chapter, the authors discuss the evidence that genetic factors, lipids, and lipoproteins, likely to be linked to both vascular disease and AD, may have an additional role in determining human longevity, with special emphasis placed on the APOE and ACE1 genes.Complex inter-relationships between age-associated illnesses such as vascular disease and Alzheimer’s disease (AD) suggest that biological and genetic pathways may be worthy of examination in centenarian populations to provide insights into human longevity. The search for factors involved in aging and longevity has progressed extensively in the recent years because of increased human life expectancy and elevation of the number of elderly people. Different genetic and non genetic factors have been examined in the quest to understand the biological basis of human longevity. Indeed, it can be hypothesised that centenarians have environmental and genetic factors that confer unexpected survival advantage. Examples of such advantage are characterized by marked delay or escape from age-related diseases, such as coronary artery disease (CAD), cerebrovascular disease (CVD), and AD, respectively, the first, the third, and the fourth largest causes of mortality, in the western populatio n. Th us one can suggest that genes and biochemical factors likely to be implicated in these disorders may have a role in human longevity. In this chapter, the authors discuss the evidence that genetic factors, lipids, and lipoproteins, likely to be linked to both vascular disease and AD, may have an additional role in determining human longevity, with special emphasis placed on the APOE and ACE1 genes
Genetics of late-onset Alzheimer's disease: vascular risk and beta-amyloid metabolism
No full textProgress in clinical and basic research of Alzheimer's disease (AD) suggested theoretical models of possible pathogenetic mechanisms, with a primary role of the genetic factors that have been implicated in AD. These can be divided into two main categories. First, the three genes in which mutations are known to result in early onset autosomal dominant familial AD (presenilins 1 and 2, and amyloid beta protein precursor [APP]): well characterized but that account for only a small proportion of AD cases. Secondly, late onset, sporadic AD is more common and evidence suggests that there is a genetic component to this type of disease. A number of genetic risk factors have been implicated that might increase the risk of developing sporadic disease: particularly, apolipoprotein E (apo E) polymorphism and many others suggested by linkage studies [α-macroglobulin, low density receptor protein (LRP1), bleomycin hydrolase], with a precise role in β-amyloid metabolism and deposition. Many of these are controversial and studies have shown conflicting results, but apoE polymorphism seems to be only one of the possible genetic factors suggested to play a role in the multifactoral pathogenesis of AD. Regional and ethnic differences may affect the strenght of association between apoE ε4 allele and the disease, and we reported evidences of the decreasing frequency of ε4 allele in AD patients and centenarians from Northern to Southern European regions. Finally, several genetic risk factors of vascular origin (angiotensin converting enzyme, methyltetrahydropholate-reductase, and NOS3 gene polymorphisms) have been implicated in the development of both vascular dementia and AD with conflicting results
Interleukin 6-174 G/C promoter gene polymorphism in centenarians: no evidence of association with human longevity or interaction with apolipoprotein E alleles.
No full textThe C allele at position 2174 in the promoter of the interleukin 6 (IL-6) gene has been associated with reduced gene expression and
reduced plasma levels of IL-6. Given that IL-6 tracks with functional disability and age-related diseases, there may be attrition or reduction in
the frequency of the homozygous subjects, who produce higher IL-6 serum levels, in older survivors in a population. In fact, a marked
reduction of the IL-6*G/*G genotype was recently demonstrated in male though not female Italian centenarians compared with younger age groups. First aim of the present study was to investigate whether there was evidence of an association among IL-6 2174 G/C promoter polymorphism and extreme longevity in a population of 81 centenarians compared with a control group of 122 middle-aged healthy subjects (mean age: 51 ^ 18 SD; range: 19–73 years), from Apulia (Southern Italy). Secondly, we also tested possible interaction of apolipoprotein E (APOE) alleles with the IL-6 2174 G/C promoter polymorphism in view of our recent findings for reduced APOE 14 allele in centenarians. No differences have been found in the IL-6 2174 G/C promoter allele and genotype frequencies between centenarians and controls nor was there any observed interaction with APOE alleles that are also reputed to be linked to longevity. Regional genetic differences in conjunction with differing environmental factors may explain in part previous results suggesting a role of this polymorphism in longevity
Interleukin 6 variable number of tandem repeats (VNTR) gene polymorphism in centenarians
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Cerebrovascular disease in the elderly: Lipoprotein metabolism and cognitive decline [Malattiacerebrovascolare nell'anziano: Metabolismo lipoproteico e declino cognitivo]
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Whole-diet approach, Mediterranean diet, and Alzheimer disease.
No full textVery recently, Scarmeas and colleagues reported the results of a community-based study involving 2258 nondemented individuals in New York in which adherence to a traditional Mediterranean diet (MeDi) was associated with significant reduction in risk for incident Alzheimer disease. Scarmeas and colleagues used in this report a scale indicating the degree of adherence to the traditional MeDi: a value of 0 or 1 was assigned to each of 9 indicated components with the use of the sex-specific median as the cut-off.However, in the study of Scarmeas and colleagues, the ratio of the median daily intake of monounsaturated fatty acids to saturated fatty acids (one of the hallmarks of the MeDi) for individual food categories by MeDi score tertiles was <1 and overall about times lower than the same value calculated from other studies on MeDi.In the last years, the study approach was to associate single micronutrients or macronutrients to age-related cognitive decline, mild cognitive impairment, Alzheimer disease, or vascular dementia. Findings from the Italian Longitudinal Study on Aging demonstrated that in a 8.5-year follow-up, high monounsaturated fatty acid, polyunsaturated fatty acid, and total energy intake was significantly associated with a better cognitive performance in time.5 Furthermore, in the same sample, high intake of polyunsaturated fatty acids appeared to have a borderline nonsignificant trend for a protective effect against the development of mild cognitive impairment
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