Contribution of alcohol use disorders to the burden of dementia in France 2008–13: a nationwide retrospective cohort study

Schwarzinger, Michaël; Pollock, Bruce G.; Hasan, Omer Syed Muhammad; Dufouil, Carole; Rehm, Jürgen; Baillot, Sylvain; Guibert, Q; Planchet, Frédéric; Luchini, Stéphane

doi:10.1016/s2468-2667(18)30022-7

Cited by 251 publications

(212 citation statements)

References 29 publications

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“…The YLLs for Alzheimer’s disease and all forms of dementia are relatively small in absolute terms, as these diseases often occur late in life. However, a recent analysis of French hospitalization data in more than 30 million patients revealed, that while the overall alcohol-attributable fraction for dementia was low, more than 50% of all early onset dementias (defined as onset before age 65 years) were either alcohol-related dementias [52, 53], or in people with alcohol use disorders [54]. In other words, in the age groups impacting life expectancy, alcohol was a major risk factor for all types of dementia.…”

Section: What Causes Of Death Were Associated With Increases In Premamentioning

confidence: 99%

Decreases of Life Expectancy Despite Decreases in Non-Communicable Disease Mortality: The Role of Substance Use and Socioeconomic Status

Rehm

Probst

2018

Eur Addict Res

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With the epidemiological transition, causes of death shifted from communicable to non-communicable diseases (NCDs) and life expectancy increased, as these NCD deaths occurred later in life. However, in the United States, over the past years, life expectancy has been stagnating or decreasing despite decreasing NCD mortality rates. Analyses of the most important underlying causes of death with increasing premature mortality reveal that psychoactive substance use played a crucial role for these increases. Furthermore, it can be shown, that a high proportion of the increased premature mortality and decreased life expectancies happened in lower socio-economic strata. Substance use policies should thus focus on lowering the gap between substance-attributable mortality in higher versus lower socioeconomic strata.

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Section: What Causes Of Death Were Associated With Increases In Premamentioning

confidence: 99%

Decreases of Life Expectancy Despite Decreases in Non-Communicable Disease Mortality: The Role of Substance Use and Socioeconomic Status

Rehm

Probst

2018

Eur Addict Res

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“…Alcohol use disorders (AUD) have been associated with the development of cognitive impairment and different forms of dementia [1][2][3], and excessive as well as prolonged alcohol use is known to lead to permanent damage of structure and function of the brain [2,4]. Different pathophysiological mechanisms of neurotoxicity of alcohol have been proposed such as glutamate excitotoxicity, oxidative stress, and disruption of neurogenesis [1,2,5].…”

Section: Introductionmentioning

confidence: 99%

Thiamine Substitution in Alcohol Use Disorder: A Narrative Review of Medical Guidelines

et al. 2019

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Aims: Patients with alcohol use disorder (AUD) frequently suffer from cognitive deficits ranging from mild symptoms to most severe forms. Wernicke encephalopathy (WE), caused by thiamine deficiency, is a potentially fatal syndrome characterized by the clinical triad of ophthalmoplegia, ataxia, and confusion. WE frequently presents in patients with AUD and, if left untreated, can progress to Wernicke-Korsakoff syndrome, which constitutes severe anterograde amnesia, confabulation, and behavioral abnormalities. Due to oftentimes indistinct clinical presentation, WE remains undiagnosed in up to 80% of cases. We conducted a review of current treatment guidelines for AUD in order to identify recommendations for the use of thiamine. Methods: Three different keyword combinations (“alcohol treatment guideline,” “alcohol withdrawal guideline,” and “alcohol treatment recommendation”) were entered in PubMed and Scopus, additional guidelines were searched screening the online sites of the respective agencies or societies. In total, 14 guidelines were included. Results: Thiamine was mentioned in all but one of the reviewed publications. Specifications on application modalities and indications varied considerably. While the majority of reviewed guidelines recommended parenteral thiamine only for patients at high risk for WE, some gave no information regarding the application form or dosage. Conclusion: Substitution of parenteral thiamine in individuals with suspected WE is a well-established treatment regimen. However, suggestions according to guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with AUD. Further research is of utmost importance to raise awareness for this potentially undervalued problem.

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“…Whatever the reason, the similarities between AD and ARBD just described would seem to provide the most obvious reason why heavy drinking appears to be associated with a higher risk of developing Alzheimer's and other dementias (Anttila et al, 2004;Järvenpää et al, 2005;Kim et al, 2012;Schwarzinger et al, 2018;Sabia et al, 2018). The fact that people with the ApoE4 allele appear to have a much greater risk of developing dementia as a result of drinking ethanol (including even light-to-moderate drinking), compared with non-carriers of the allele (Dufouil et al, 2000;Mukamal et al, 2003;Anttila et al, 2004;Kim et al, 2012;Downer, Zanjani & Fardo, 2014), would seem only to add further weight to this association.…”

Section: Basal Forebrain Damage In Ad and Arbdmentioning

confidence: 99%

A lipid-leakage model for Alzheimer’s Disease

Rudge

2019

Preprint

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This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-leakage model. It proposes that AD is caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principle role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-leakage model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that best accounts for all currently known major risk factors, and credibly explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that have been too readily overlooked by other accounts of this disease.

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Contribution of alcohol use disorders to the burden of dementia in France 2008–13: a nationwide retrospective cohort study

Abstract: None.

Cited by 251 publications

References 29 publications

Decreases of Life Expectancy Despite Decreases in Non-Communicable Disease Mortality: The Role of Substance Use and Socioeconomic Status

Decreases of Life Expectancy Despite Decreases in Non-Communicable Disease Mortality: The Role of Substance Use and Socioeconomic Status

Thiamine Substitution in Alcohol Use Disorder: A Narrative Review of Medical Guidelines

A lipid-leakage model for Alzheimer’s Disease

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