Not just the hangover
The "hangover gene" is the cause of not only "alcoholic blush", but also the development of senile dementia
According to experts, by the middle of the century, Alzheimer's disease – the most common form of senile dementia – will affect more than 150 million people. It turned out that the development of this disease is facilitated by a frequently occurring mutation in a gene that is involved in alcohol metabolism, according to a press release from Stanford University School of Medicine Alcohol, ‘Asian glow’ mutation may contribute to Alzheimer's disease, study finds.
No one disputes that alcohol (ethanol) is a toxic substance. WHO assesses it as the third most important global health risk factor, increasing the likelihood of chronic diseases, including in developed countries. For example, the main metabolite of ethanol in the body – the infamous acetaldehyde, which causes a hangover, is a carcinogen. But his "dirty business" in the body is not limited to this.
Acetaldehyde is formed as a result of incomplete decomposition of ethyl alcohol. And this toxic substance decomposes under the influence of the enzyme aldehyde dehydrogenase 2 (ALDH2), located in special "energy" structures of the cell – mitochondria. At the same time, it is known that acetaldehyde damages the mitochondria themselves and disrupts their work due to increased oxidative stress in cells. This creates a vicious circle: the more mitochondria are damaged, the worse the enzyme designed to fight acetaldehyde works, and the more free radicals are formed. The result may be the death of the cell.
A mutation is known in the gene encoding the enzyme ALDH2, which significantly reduces its activity. In carriers of this mutation, acetaldehyde accumulates in the body more than usual, which causes a characteristic redness of the face, which is also called "Asian blush", since this mutation is most common in East Asians (up to 45% compared to 8% of the world population as a whole).
Recently, scientists from Stanford University (USA) We decided to check the contradictory data concerning a possible link between a mutation in the ALDH2 gene and the development of Alzheimer's disease. The experiments used cell cultures of fibroblasts (connective tissue cells) of people suffering from hereditary Alzheimer's disease and having a mutation in the ALDH2 gene, and mice with a mutation in the same gene. Alcohol was added directly to the culture, and it was injected into animals for 11 weeks at a dose simulating two standard "drinks" per day for a person (one "drink" is about a large mug of beer, or 150 ml (glass) of wine, or 45 ml of forty–degree alcohol).
It turned out that the experimental fibroblasts initially had an increased level of free radicals and impaired mitochondrial functions, and the effect of ethyl alcohol aggravated these manifestations. The brain cells of the "drinking" mutant mice were characterized by the same phenomena. In addition, they accumulated more of the pathological protein beta-amyloid, characteristic of Alzheimer's disease, and there were signs of inflammation, which may increase the progression of this disease.
The scientists confirmed the results with the help of a substance discovered in 2008 that can bind to the mutant protein ALDH2 and restore its function. The introduction of this compound to experimental mice treated with alcohol led to a decrease in the accumulation of toxic proteins and the restoration of free radical levels.
Thus, people with a mutation in the ALDH2 gene should be aware that drinking alcohol is fraught for them not only with a severe hangover, but also with the risk of developing Alzheimer's disease. By the way, the same phenomena, albeit on a smaller scale, threaten all other "consumers". In any case, the results of this study open up new directions in the fight against senile dementia and serve as another argument for supporters of a sober lifestyle.
Article by Joshi et al. Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer's disease related pathology is published in the journal Acta Neuropathologica Communications.
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