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Alcohol is toxic to neurons and can cause their loss, brain damage, and cognitive decline. Epidemiological studies have identified a link between ethanol consumption and over 200 somatic diseases. Despite this, it remains the most common legal drug in the world and is an integral part of the social fabric in many cultures.
Thanks to modern tools, British and Spanish researchers have managed to understand the long-term impact of alcohol on mature neurons and neuroblasts, which are underdeveloped neural cells.
The study was published in the journal Antioxidants.
Alcohol: Accessible and Dangerous
The link between alcohol and harm to humans is complex and multidimensional, increasing uniformly with higher consumption. Considering the years of life adjusted for disability, more than 5.1% of the total burden of diseases and injuries is caused by ethanol. It kills quite swiftly: approximately 13.5% of people aged 20–39 die from alcohol-related causes.
The negative impact of alcohol abuse has been demonstrated by numerous studies. Despite the existence of opinions that small, infrequent doses may have a positive effect on brain health, the negative consequences far outweigh the benefits. Scientists have proven that alcohol leads to a reduction in both white and/or gray matter in the brain, causing cognitive decline and dementia.
Children, adolescents, and the elderly are particularly susceptible to the toxic effects of ethanol. Consumption during pregnancy affects the neurodevelopment of the fetus and leads to fetal alcohol spectrum disorders. A child may be born with serious neurological and cognitive impairments.
Differentiated and Undifferentiated Cells
Scientists investigated the toxic effects of alcohol on undifferentiated (neuroblasts) and differentiated (mature neurons) neural cells. An artificially cultured cell line was purchased for the study from the European Collection of Authenticated Cell Cultures. Postmortem brain tissue from individuals dependent on alcohol was provided by the Neuropsychopharmacology Research Group at the Department of Pharmacology, University of the Basque Country, Spain.
The artificially cultured cells were exposed to 0–200 millimoles (mM) of ethanol for 3, 6, 12, or 24 hours. They were then examined using a wide range of analyzes and tests. These included quantification of cell viability, assessment of mitochondrial morphology and functionality, production of reactive oxygen species, and cellular accumulation of oxidatively damaged proteins. Postmortem brain tissues from alcoholics were also analyzed.
Damage Accumulates Over Time
Alcohol significantly reduces the viability and metabolic activity of both undifferentiated and differentiated neural cells. This negative impact increases linearly with higher ethanol concentrations and longer exposure durations. The lowest concentration studied (10 mM) slightly increased the metabolic activity of the cells, though the effect was minimal.
However, consumption during neurodevelopment is particularly detrimental to undifferentiated cells. Differentiation makes cells more resistant to ethanol, requiring higher concentrations to reduce viability. Despite this, mature neurons are more susceptible to alcohol-induced oxidative protein damage. The characteristics of the artificially cultured proteins in the study resemble those found in postmortem brain tissues of adults.
Thus, according to scientists, alcohol kills cells at all developmental stages. Rapidly: immature cells that have yet to develop into functional cells. Slowly: mature neurons, gradually decreasing their functionality through oxidative stress.
