The effect of alcohol and tobacco consumption, and apolipoprotein E genotype, on the age of onset in Alzheimer's disease

Harwood, Dylan G.; Kalechstein, Ari D.; Barker, Warren W.; Strauman, Silvia; George-Hyslop, Peter St; Iglesias, Casandra; Loewenstein, David; Duara, Ranjan

doi:10.1002/gps.2372

Cited by 91 publications

(77 citation statements)

References 42 publications

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“…Individuals who are homozygous for the ApoE4 allele develop Alzheimer's disease earlier at a mean age of 70 years. Furthermore, individuals homozygous for the ApoE4 allele, as well as tobacco smokers and heavy alcohol consumers are more likely to be diagnosed with Alzheimer's disease approximately 10 years earlier than those with none of these three risk factors [139]. The ApoE4 allele is also a risk factor for hypercholesterolemia.…”

Section: Amyloid-β and Apoe-epsilon 4 Allelementioning

confidence: 99%

Wine consumption, cognitive function and dementias – A relationship?

Stockley

2016

NUA

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Abstract. Healthy cognitive function is essential for quality of life, wellbeing and independent living, and is negatively associated with dementias. A series of longitudinal and neuro-imaging studies in the elderly have shown that light to moderate wine consumption is neuro-protective although heavy or abusive alcohol consumption is neuro-toxic. A J-shaped relationship between alcohol consumption, cognitive dysfunction and risk of dementias is also observed for younger and middle aged consumers. There is also no data to suggest that long-term light to moderate alcohol consumption exacerbates age-related cognitive decline and impairment. An optimal amount of wine for neuro-protection appears to be up to 30 g alcohol daily.There are multiple plausible biological mechanisms in various animal models, in vitro and in vivo for wine-derived phenolic compounds which go beyond their antioxidant activity and attenuation of oxidative stress.

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Section: Amyloid-β and Apoe-epsilon 4 Allelementioning

confidence: 99%

Wine consumption, cognitive function and dementias – A relationship?

Stockley

2016

NUA

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“…29 30 Moderate consumption of alcohol has been observed to be a protective factor in non-ApoE ε4 carriers, 31 32 whereas heavy drinking may lower the age of onset of Alzheimer's disease. 33 Caffeine consumption has been associated with a reduction in density of white matter lesions and possible delaying of onset of dementia, 34 and inadequate consumption of water has been observed to increase risk. 35 Nicotine intake has also been observed to decrease the risk of dementia, 36 although more recent studies have suggested that it may increase it and also bring forward age of onset with an ApoE ε4 interactive effect.…”

Section: Candidate Exposuresmentioning

confidence: 99%

Designing prevention programmes to reduce incidence of dementia: prospective cohort study of modifiable risk factors

Ritchie

Carrière

Ritchie

et al. 2010

BMJ

201

171

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Objective To estimate the percentage reduction in incidence of dementia that would be obtained if specific risk factors were eliminated. Design Prospective seven year cohort study. Setting General population, Montpellier, France. Participants 1433 people aged over 65 with a mean baseline age of 72.5 (SD 5.1) years. Main outcome measures Diagnosis of mild cognitive impairment or dementia established by a standardised neurological examination. Results Cox models were constructed to derive hazard ratios and determine confounding and interaction effects for potentially modifiable risk factors for dementia. Mean percentage population attributable fractions were calculated with 95% confidence intervals derived from bootstrapping for seven year incidence of mild cognitive impairment or dementia. The final model retained crystallised intelligence (population attributable fraction 18.11%, 95% confidence interval 10.91% to 25.42%), depression (10.31%, 3.66% to 17.17%), fruit and vegetable consumption (6.46%, 0.15% to 13.06%), diabetes (4.88%, 1.87% to 7.98%), and apolipoprotein E ε4 allele (7.11%, 2.44% to 11.98%). Conclusions Increasing crystallised intelligence and fruit and vegetable consumption and eliminating depression and diabetes are likely to have the biggest impact on reducing the incidence of dementia, outweighing even the effect of removing the principal known genetic risk factor. Although causal relations cannot be concluded with certainty, the study suggests priorities that may inform public health programmes. INTRODUCTIONThe past 30 years have seen the proliferation of methodologically well constructed prospective population studies of dementia that have pointed to multiple risk factors. Although the exact cause of the dementias remains unknown, these studies together suggest a complex interaction of exposures that contribute differentially to the probability and timing of onset of disease. The contribution of epidemiology to dementia research has, however, been principally in the areas

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“…It has been described in south Asian men a higher risk to develop CHD as compared to men from other genetic backgrounds [30,31]. Furthermore, cigarette smoking is positively correlated to CHD [1] and to Alzheimer's Disease [28,29].…”

Section: Discussionmentioning

confidence: 99%

“…As positive correlations between cigarette smoking and Alzheimer's Disease have been identified [28,29], the aim of the present study was to investigate the plasma and erythrocyte membrane phospholipid fatty acid profiles of young adult males of Indian, Sri-Lankan or Bangladeshi genetic backgrounds with a smoking habit. The population recruited is relatively young and smokes between 20 and 60 cigarettes per week.…”

Section: Introductionmentioning

confidence: 99%

Perturbations in Blood Phosphatidylcholine and Sphingomyelin Fatty Acid Composition in a Sample Population of Cigarette Smokers

2013

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Docosahexaenoic (DHA) and arachidonic acids (AA) are polyunsaturated fatty acids (PUFAs), major components of brain tissue and neural systems, and the precursors of a number of biologically active metabolites with functions in inflammation resolution, neuroprotection and other actions. As PUFAs are highly susceptible to peroxidation, we hypothesised whether cigarette smokers would present altered PUFAs levels in plasma and erythrocyte phospholipids. Adult males from Indian, Sri-Lankan or Bangladeshi genetic backgrounds who reported smoking between 20 and 60 cigarettes per week were recruited. The control group consisted of matched non-smokers. A blood sample was taken, plasma and erythrocyte total lipids were extracted, phospholipids were separated by thin layer chromatography, and the fatty acid content analysed by gas chromatography. In smokers, dihomo-gamma-linolenic acid, the AA precursor, was significantly reduced in plasma and erythrocyte phosphatidylcholine. AA and DHA were significantly reduced in erythrocyte sphingomyelin. Relatively short term smoking has affected the fatty acid composition of plasma and erythrocyte phospholipids with functions in neural tissue composition, cell signalling, cell growth, intracellular trafficking, neuroprotection and inflammation, in a relatively young population. As lipid peroxidation is pivotal in the pathogenesis of atherosclerosis and neurodegenerative diseases such as Alzheimer disease, early effects of smoking may be relevant for the development of such conditions.

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The effect of alcohol and tobacco consumption, and apolipoprotein E genotype, on the age of onset in Alzheimer's disease

Abstract: The results suggest that APOE epsilon4 and heavy drinking and heavy smoking lower the age of onset for AD in an additive fashion.

Cited by 91 publications

References 42 publications

Wine consumption, cognitive function and dementias – A relationship?

Wine consumption, cognitive function and dementias – A relationship?

Designing prevention programmes to reduce incidence of dementia: prospective cohort study of modifiable risk factors

Perturbations in Blood Phosphatidylcholine and Sphingomyelin Fatty Acid Composition in a Sample Population of Cigarette Smokers

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