The relationship between AD, dementia and alcohol use/abuse has been the subject of many studies with varying and conflicting results. It is still unclear whether light to moderate alcohol consumption can lead to dementia or whether alcohol consumption can reduce the risk of developing AD [
49]. Numerous published data confirm that low to moderate alcohol consumption, including wine (part of the Mediterranean diet), which contains numerous polyphenols which have protective effects, including minimising the effects of oxidative stress, inhibiting β-amyloid deposition, significantly reduces the risk of dementia and the risk of AD [
50]. However, excessive amounts of ethanol increase the accumulation of Aβ and tau protein phosphorylation, contributing to the development of Alzheimer’s disease. Observational studies indicate that high alcohol consumption leads to a deterioration of cognitive and executive functions and leads to alcoholic dementia. The link between alcohol consumption and cognitive decline is believed to be “J” or “U” shaped [
51]. In contrast, light/moderate alcohol consumption is associated with a reduced risk of dementia in individuals aged 55 years or older [
52]. Regarding the type of alcoholic beverage, the Ritinberg study [
52] found no difference between wine, beer or liquor. It is believed that beer (which is a component of the Mediterranean diet) and its ingredients (carbohydrates, protein/amino acids, minerals, vitamins and other compounds, such as polyphenols) exert a beneficial effect in the prevention of Alzheimer’s disease. Regular consumption of beer, or low-alcohol or non-alcoholic beer, can prevent AD and other neurodegenerative diseases as it effectively reduces the accumulation of aluminium in the body and also alleviates the mineral imbalance in the body and the brain and the pro-oxidative and pro-inflammatory effects caused by aluminium [
31]. While the Luchsinger study [
53] found that only wine (particularly red) has the strongest protective effect because resveratrol, a sirtuin 1 activator and other polyphenols present in the grapes of red wine reduce Aβ plaque burden and improve cognitive function. It has been noted that resveratrol actually reduces the levels of Aβ40 and Aβ42 in cerebrospinal fluid, but at the same time, it accelerated brain atrophy [
54]; further studies are needed to confirm these results. Surprisingly, heavy drinking in late life has no effect on dementia risk compared to non-drinkers [
52,
55], but heavy drinking in adolescence is associated with damage to the prefrontal cortex and the hippocampus, and with neurocognitive dysfunction, it increases the risk of alcoholic dementia, similar to AD [
49]. Importantly, alcohol misuse is also associated with a number of other disorders. Many publications state that ethanol and its metabolites not only have neurotoxic effects but directly exert toxic effects on the mucous membranes of the mouth (including periodontium), oral cavity, throat, oesophagus, liver, stomach, pancreas, kidney and can cause lung cancer (especially in cigarette smokers) and that regular drinking (even in small amounts) can lead to alcohol dependence [
56,
57].
Many studies support the benefits of low to moderate alcohol consumption in preventing AD [
52]. However, these results should be considered insufficient to suggest that long-term abstinence should consider alcohol consumption in their diet to prevent AD risk. In addition, other risk factors (in addition to binge drinking), such as smoking or abusing other substances, can play an important role in the development and progression of many diseases, including neurodegenerative diseases. We believe that light to moderate alcohol consumption may be important in preventing AD.