Alcohol has been examined as a risk factor

Alcohol has been examined as a risk factor selleck chem Calcitriol for other dementia syndromes. There are suggestions of a U- or J-shaped relationship between alcohol consumption and dementia, with low-moderate drinking levels reducing the risk of overall dementia but heavy use increasing the risk [14]. Low to moderate alcohol use is thought to reduce the risk of coronary artery disease and ischemic stroke through the inhibitory effect of ethanol on platelet aggregation and reduction of inflammatory markers and by alteration of the serum lipid profile [36]. The anti-oxidant effect of polyphenols or ethanol itself might also provide neuroprotection [14]. Alternatively, heavier drinking may contribute to adverse cerebrovascular changes (hypertension and raised triglycerides) and increased risk of arterial thrombosis, cardiac disorders, and strokes [6].

A meta-analysis examining the association of ethanol and incident dementia concluded that small amounts of alcohol likely protects against Alzheimer’s disease but not against vascular dementia [37]. However, others suggest that the benefit of moderate drinking applies to all forms of dementia [38]. This uncertainty was emphasized in a recent 20- year study (n = 1,300 women at least 65 years old), which reported that moderate alcohol consumption was not protective against dementia. Furthermore, women who increased their alcohol consumption over the course of the study had an increased risk of developing dementia [39].

Interestingly, animal models have shown that low concentrations of alcohol protect cultured cortical and hippocampal neurons against the synapse damage induced by amyloid-?? and ??-synuclein, providing a pathological explanation for reports that alcohol consumption protects against the development of specific dementia syndromes [40]. Nosology? The current DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th edition) criteria for ‘alcohol-induced persisting dementia’ specify the persistence of cognitive and functional decline following cessation of alcohol consumption, with all other causes of dementia excluded [41]. Oslin and colleagues [35] attempted to improve the validity and reliability of ARD diagnosis by standardizing alcohol consumption criteria for a ‘probable’ diagnosis of ARD (length and severity of alcohol use) and specifying a minimum abstinence time for a dementia diagnosis to be considered.

These guidelines were not meant to be definitive and were designed with the intention of stimulating further research. Even so, further use of their criteria has been limited to a handful of studies Drug_discovery [42-44] that have inconsistently adopted elements of the criteria (for example, some have excluded participants with previous BI 6727 acute symptomatology of WKS) and differed in participants’ ages, education level, and global cognitive function. Thus, current diagnostic criteria for ARD have been inadequately tested.

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