Is it true that alcohol kills neurons in the brain?

How does the consumption of alcoholic beverages affect nerve cells?

One of the main and most recent objectives of neurology has been to study the toxic or harmful effects of psychotropic substances on the brain. Through different investigations it has been possible to know some of the consequences of excessive consumption of chemical compounds such as ethanol.

From there, it has become the belief that alcohol kills neurons has become very popular.To what extent is it true? Let's see it in the following text.

How do neurons die?

To begin with we will remember briefly the vital cycle of the neurons and what we understand by "neuronal death". As occurs with the different cell populations that make up our organism, nerve cells (neurons) act by a proliferation mechanism that includes cell loss, renewal and differentiation.

The death of a cell is defined as the arrest of its Biological processes due to irreversible morphological, functional and biochemical modifications that prevent it from carrying out its vital functions (Sánchez, 2001). In this sense, neuronal death is considered to have occurred when a nerve cell loses the capacity to establish adequate interstitial connections.

Two major types of neuronal death

Neuronal death is when its characteristics are significantly modified, preventing the ability to function. And the latter does not necessarily correspond to a decrease in the volume of cells within the affected areas. Let us now consider the two main types of neuronal death:

1. apoptosis

Also known as programmed neuronal death. It has adaptive purposes, i.e., it serves to maintain only the most frequently used connections and occurs especially in the early years of development. occurs especially in the first years of development.

2. Necrosis

Consists of the loss of the neuron's functions due to the influence of external factors. In this process the cells are not always phagocytized (i.e. they do not disintegrate). (i.e. they do not disintegrate completely within the organism, which can lead to other medical complications), but they are considered dead because they lose the capacity to be activated and to produce connections among themselves.

Having said this, we will see what is the toxic mechanism produced by alcohol consumption and whether the latter has the capacity to generate a process of apoptosis or necrosis.

Toxic mechanism of frequent alcohol consumption

The toxic effects of ethanol (recreational alcohol) vary according to the specific region of the brain on which they act. Also vary according to age or stage of development, dose, and duration of exposures..

When it comes to the mature brain, chronic or intense exposure to ethanol can cause different diseases, both of the central nervous system and the peripheral nervous system, as well as skeletal muscle (de la Monte and Krill, 2014).

The consequence is that, in the long term, excessive alcohol consumption significantly impairs executive functions. In other words, alcohol can produce a degenerative activity of the nervous system, as it gradually impairs the function of neurons, including neuronal survival capacity, cell migration and glial cell structure. While the latter does not necessarily mean that the neurons necessarily disintegrate, it can imply the the definitive loss of their functions, which falls under the definition of neuronal death, but it may imply the definitive loss of their functions, which falls under the definition of neuronal death..

This is because, among many other things, excessive alcohol consumption causes thiamine deficiency, which is a vitamin of the B complex, essential in the conduction of nerve signals and in supplying energy to the brain.

Thiamine deficiency reduces protein levels in the thalamus and also modifies neurotransmitter levels. and also modifies the levels of neurotransmitters in the hippocampus and cerebral cortex. As a consequence, it produces alterations in special memory and increases perseverative behavior. Also, some of the long-term consequences include the loss of functions necessary for neuronal plasticity and survival.

Peri- and postnatal alcohol exposure

There is a large body of scientific literature reporting several of the consequences of frequent alcohol exposure, both in the late perinatal period and in the early years of life (the period in which human brain formation takes place).

It is during the early stages of postnatal development that an explosion of synaptogenesis, the formation of synapses or connections between neurons, occurs. Several studies agree that ethanol (which has antagonistic properties of glutamate receptors -the main excitatory neurotransmitter in the brain-), triggers a harmful and generalized process of apoptosis.. This is because such antagonist activity favors excitotoxic neurodegeneration and abnormal inhibition of neuronal activity.

In other words, ethanol prevents the passage of glutamate, which in turn inhibits the formation of synapses, favoring an unnecessary process of programmed neuronal death. This has been accepted as one of the possible explanations for the reduction of brain mass and human fetal alcohol syndrome in newborns.

It is worth mentioning that neuronal immaturity, characteristic of the first years of human development, is especially sensitive to different environmental agents, is particularly sensitive to different environmental agents that can generate harmful modifications in synaptic connections. Ethanol is one of these agents, but it is not the only one, and it can also come from different sources, often external to the pregnancy itself or to the child.

Some harmful effects of alcohol in pregnancy

According to Suzanne M. de la Monte and Jillian J. Kril (2014), the causes of brain degeneration and atrophy in people with alcoholism is continually being debated in the scientific community..

In their review on Alcohol-Related Human Neuropathology, published in the journal Acta Neuropathologica, they tell us that the main tissues that prolonged alcohol consumption affects in the mature brain are the following: purkinje and granular cells, and white matter fibers. We will briefly explain what this consists of.

1. Decrease of the white matter

The most visible and well-studied deleterious reaction of the brains of people who have consumed alcohol to excess is white matter depletion. The clinical manifestations that derive from this range from subtle or undetectable impairment, to cognitive impairment with significant deficits in executive functions.. Scientific findings suggest that cortical atrophy resulting from excessive alcohol consumption is associated with a definite loss of synapses or significant impairment of their functions.

2. Granule cells and Purkinje cells

Granule cells are the smallest cells in the brain. They are found in different parts of the cerebellum, adjacent to the purkinje cells, which are a type of neuron known as GABAergic. The latter are some of the largest neurons that have been located so far.

Among other things, they are responsible for regulating sensory and motor functions. Regular alcohol consumption lasting between 20 to 30 years results in a 15% reduction of Purkinje cells, while high consumption during the same years results in 33.4 % (de la Monte and Kril, 2014). The degeneration of these cells in the vermis (space dividing the two cerebral hemispheres) correlates with the development of ataxia; while their loss in the lateral lobes has been related to cognitive alterations.

In summary

In summary, we can say that alcohol can generate both momentary and permanent impairment in the activity of nerve cells, as a result of important modifications in the structure of these cells and in their capacity to establish communication.

To a large extent the severity of the impairment depends on the duration of exposure to alcohol, as well as the age of the person and the specific area of the brain where the damage has occurred.

If the damage is permanent, then it is neuronal death, but this has only been studied in the case of people whose ethanol consumption is not only recreational, but also in the case of people who drink ethanol for recreational purposes. people whose ethanol consumption is not only recreational, but also excessive and prolonged. Likewise, the programmed loss of neuronal activity due to exposure to alcohol during the perinatal period and in organisms with few years of life has been studied.

In the case of excessive and prolonged consumption in adulthood, it is neuronal necrosis due to excitotoxicity; while in the case of exposure during perinatal and postnatal development, it is non-adaptive apoptosis. In this sense, alcohol consumed in excess for many years, as well as very early contact with this substance, can result in the death of neurons, among other detrimental health consequences.

Bibliographical references:

• De la Monte, S. & Kril, J. (2014). Human alcohol-related neuropathology. Acta Neuropathologica, 127: 71-90.
• Creeley, C. & Olney, J. (2013). Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development. Brain Sciences, 3: 1153-1181.
• Tokuda, K., Izumi, Y., Zorumski, CF. (2011). Ethanol enhances neurosteroidogenesis in hippocampal pyramidal neurons by paradoxical NMDA receptor activation. Journal of Neuroscience, 31(27): 1660-11.
• Feldstein, A. & Gores, G. (2005). Apoptosis in alcoholic and nonalcoholic steatohepatitis. Frontiers in Bioscience, 10: 3093-3099.
• He, J., Nixon, K., Shetty, A. & Crews, F. (2005). Chronic alcohol exposure reduces hippocampal neurogenesis and dendritic growth of newborn neurons. European Journal of Neuroscience, 21(10): 2711-2720.
• Olney, J. (2002). New Insights and New Issues in Developmental Neurotoxicology. NeuroToxicology, 23(6): 659-668.
• Goodlett, C. & Horn, K. (2001). Mechanisms of Alcohol-Induced Damage to the Developing Nervous System. Alcohol Research and Health. 25(3): 175-184.
• Sánchez, V. (2001). Mecanismos reguladores de la muerte celular no necrótica. Revista Cubana de Investigaciones Biomédicas, 20(4): 266-274.