25 resultados para apolipoprotein A1


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OBJECTIVES: Behavioural and psychological symptoms of dementia (BPSD) are potent predictors of carer distress and admission to institutional care. In Alzheimer's disease (AD), depressive symptoms are one of the most common complaints affecting around 50% of all patients. There is speculation these symptoms result from known genetic risk factors for AD, therefore we investigated the role of apolipoprotein E epsilon4 in the aetiology of depression in AD. METHODS: In this well-characterised cohort (n = 404) from the relatively genetically homogeneous Northern Ireland population, we tested the hypothesis that genetic variants of apolipoprotein E influence the risk for depressive symptoms in AD patients using the Neuropsychiatric Inventory (NPI-D) to determine the presence of depressive symptoms during the dementing illness. RESULTS: A total of 55% of patients exhibited a history of depression/dysphoria during the course of the illness as gathered by the NPI-D questionnaire. Forty-six percent were suffering from depression/dysphoria when the analysis was restricted to the month prior to interview. No statistically significant association between genotypes or alleles of apolipoprotein E and depression/dysphoria in AD was observed, nor was any association noted between the presence of severe symptoms and genotypes/alleles of apolipoprotein E. CONCLUSIONS: These results suggest apolipoprotein E genotype creates no additional risk for depressive symptoms in AD.

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The rising number of people with cognitive impairment is placing health care budgets under significant strain. Dementia related behavioural change is a major independent risk factor for admission to expensive institutional care, and aggressive symptoms in particular are poorly tolerated by carers and frequently precipitate the collapse of home coping strategies. Aggressive change may result from known genetic risk factors for Alzheimer's disease (AD) and therefore accompany conventional markers such as apolipoprotein E (ApoE). We tested this hypothesis in 400 moderately to severely affected AD patients who were phenotyped for the presence of aggressive or agitated behaviour during the month prior to interview using the Neuropsychiatric Inventory with Caregiver Distress. The proportion of subjects with aggression/agitation in the month prior to interview was 51.8%. A significantly higher frequency of the e4 allele was found in individuals recording aggression/agitation in the month prior to interview (chi2 = 6.69, df = 2, p = 0.03). The additional risk for aggression/agitation conferred by e4 was also noted when e4 genotypes were compared against non-e4 genotypes (chi2 = 5.45, df = 1, p = 0.02, OR = 1.60, confidence interval (CI) 1.06 to 2.43). These results indicate that advanced Alzheimer's disease patients are at greater risk of aggressive symptoms because of a genetic weakness in apolipoprotein E.

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Energy levels, radiative rates, collision strengths, and effective collision strengths for all transitions up to and including the n = 5 levels of AlXIII have been computed in the j j coupling scheme including relativistic effects. All partial waves with angular momentum J less than or equal to 60 have been included, and resonances have been resolved in a fine energy grid in the threshold region. Collision strengths are tabulated at energies above thresholds in the range 170.0 less than or equal to E less than or equal to 300.0 Ryd, and results for effective collision strengths, obtained after integrating the collision strengths over a Maxwellian distribution of electron velocities, are tabulated over a wide temperature range of 4.4 less than or equal to log T-e less than or equal to 6.8 K. The importance of including relativistic effects in a calculation is discussed in comparison with the earlier available non-relativistic results.

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Piclavines AI and A2 have been synthesised for the first time. The route is short with the key step being the reaction of a bicyclic N-acyl iminium ion with 3-trimethysilyl-1-decene. This convergent strategy gave exclusively compounds in which the pendant decenyl group was axial, as a 6:1 mixture of E:Z-alkene diastereoisomers. Reduction of the lactam carbonyl group gave a 6:1 mixture of piclavines Al and A2, (C) 2000 Published by Elsevier Science Ltd.

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PURPOSE: Age-related macular degeneration (AMD) is the most common cause of blindness in older people in developed countries, and risk factors for this condition may be classified as genetic and environmental. Apolipoprotein E is putatively involved in the transport of the macular pigment (MP) carotenoids lutein (L) and zeaxanthin (Z) in serum and may also influence retinal capture of these compounds. This study was designed to investigate the relationship between macular pigment optical density (MPOD) and ApoE genotype. METHODS: This was a cross-sectional study of 302 healthy adult subjects. Dietary intake of L and Z was assessed by food frequency questionnaire, and MPOD was measured by customized heterochromatic flicker photometry. Serum L and Z were measured by HPLC. ApoE genotyping was performed by direct polymerase chain reaction amplification and DNA nucleotide sequencing from peripheral blood. RESULTS: Genotype data were available on 300 of the 302 (99.3%) subjects. The mean (+/- SD) age of the subjects in this study was 47.89 +/- 11.05 (range, 21-66) years. Subjects were classed into one of three ApoE genotype groups, as follows: group 1, epsilon2epsilon2 or epsilon2epsilon3; group 2, epsilon3epsilon3; group 3, epsilon2epsilon4 or epsilon3epsilon4 or epsilon4epsilon4. All three groups were statistically comparable in terms of age, sex, body mass index, cigarette smoking, and dietary and serum levels of L and Z. There was a statistically significant association between ApoE genotype and MPOD. Subjects who had at least one epsilon4 allele had a higher MPOD across the macula than subjects without this allele (group 1 MPOD area, 0.70 +/- 0.40; group 2 MPOD area, 0.67 +/- 0.42; group 3 MPOD area, 0.85 +/- 0.46; one-way ANOVA, P = 0.014. CONCLUSIONS: These results suggest that ApoE genotype status is associated with MPOD. This association may explain, at least in part, the putative protective effect of the epsilon4 allele for AMD and is consistent with the view that apolipoprotein profile influences the transport and/or retinal capture of circulating L and/or Z.

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The apolipoprotein (APOE) epsilon4 allele is a genetic risk factor for the development of Alzheimer's disease (AD). It has also been associated with vascular dementia (VaD) in some but not all studies. Previous studies have examined the role of APOE in predicting performance on cognitive tests in both demented and non-demented populations. In cognitively intact individuals, statistically significant group differences between APOE epsilon4 carriers and non-carriers have been demonstrated for several cognitive domains. In AD studies of the impact of APOE epsilon4 on cognition have been conflicting while no previous study has assessed cognition and impact of APOE epsilon4 in VaD. In this study we investigated the impact of APOE epsilon4 on performance in neuropsychological tests including information processing speed in patients with mild-moderate AD and VaD. We incorporated both computerized and pen and paper tests to ensure a sensitive method of assessing cognition. 109 patients participated in the study (VaD=41, AD=68). Neurocognitive performance of 44 epsilon4 present AD patients was compared to 24 epsilon4absent patients and performance of 23 epsilon4 present VaD patients was compared to 18 epsilon4 absent patients. There was evidence that APOE epsilon4 conferred a risk of poorer cognitive functioning in both patient groups. In the AD group presence of epsilon4 conferred a negative impact on some measures of speed of information processing and immediate recall while in the VaD group epsilon4 present patients had evidence of poorer accuracy on tasks such as choice reaction time and spatial working memory. In AD and VaD groups epsilon4 present patients showed impairment in selective attention. These findings provide further support of the negative impact of the epsilon4 allele in cognition.

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Factors that influence response to drug treatment are of increasing importance. We report an analysis of genetic factors affecting response to cholinesterase inhibitor therapy in 165 subjects with Alzheimer's disease (AD). The presence of apolipoprotein E e4 (APOE e4) allele was associated with early and late cognitive response to cholinesterase inhibitor treatment in mild AD (Mini-Mental State Examination (MMSE) greater than or equal to21) (P