Is it true that alcohol kills brain neurons?

One of the main and most recent goals of neurology has been to study the toxic or harmful effects of psychotropic substances in the brain. Thanks to different research, it has been possible to know some of the consequences of overconsumption of chemical compounds such as ethanol.

From here the belief that alcohol kills neurons has become very popular. How true is this? Let’s see in the following text.

    How do neurons die?

    To begin with, we will briefly remember the life cycle of neurons and what we mean by “neuronal death”. As with the different populations of cells that make up our body, nerve cells (neurons) work through a proliferation mechanism that includes cell loss, renewal and differentiation.

    The death of a cell is defined as the stopping of its biological processes by irreversible morphological, functional and biochemical changes that prevent it from fulfilling its vital functions (Sánchez, 2001). In this sense, neuronal death is considered to have occurred when a nerve cell loses the ability to make appropriate interstitial connections.

      Two main types of neuronal death

      Neuronal death is when its characteristics change significantly, hamper the ability to function. And the latter does not necessarily correspond to a decrease in the volume of cells within the affected areas. Now let’s take a look at the two main types of neuronal death:

      1. Apoptosis

      Also known as programmed neuronal death. It has adaptive purposes, that is, it serves to maintain only connections and this happens mostly in the early years of development.

      2. Necrosis

      It is the loss of neural functions due to the influence of external factors. In this process, cells are not always phagocytosed (That is, they don’t completely disintegrate in the body, which can lead to other medical complications), but are considered dead because they lose the ability to be activated and make connections with each other.

      That said, we will see what is the toxic mechanism that produces 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 depending on the specific region of the brain in which they work. too much they vary according to age or stage of development, dose and duration of exposure.

      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 of the skeletal muscle (de la Muntanya and Kril, 2014 ).

      The consequence is that in the long term, excessive alcohol consumption considerably impairs executive functions. In other words, alcohol can produce degenerative activity in the nervous system, as it gradually impairs the function of neurons, including neuronal survival capacity, cell migration, and glial cell structure. Without the latter meaning that neurons necessarily decay, yes it can lead to the permanent loss of its functions, which is part of the definition of neuronal death.

      Indeed, among other things, excessive alcohol consumption leads to a deficiency in thiamine, a complex of B vitamins, essential for conducting nerve signals and providing energy to the brain.

      Thiamine deficiency lowers protein levels in the thalamus and also alters the levels of neurotransmitters in the hippocampus and cerebral cortex. As a result, it causes special memory impairments and increases persevering behavior. In addition, some of the long-term consequences include the loss of functions necessary for plasticity and neuronal survival.

      Exposure to alcohol during the peri and postnatal period

      There is an abundant scientific literature which reports several of the consequences of frequent exposure to alcohol, both in the later stages of the perinatal period and in the first years of life (the period during which training takes place over the human brain).

      It is during the early stages of postnatal development that an explosion of synaptogenesis occurs, the formation of synapses or connections between neurons. 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. Indeed, this antagonist activity promotes excitotoxic neurodegeneration and abnormal inhibition of neuronal activity.

      To put it another way, ethanol prevents the passage of glutamate, which in turn inhibits synapse formation, promoting an unnecessary process of programmed neuronal death. The above has been accepted as one of the possible explanations for reduced brain mass and human fetal alcohol syndrome in newborns.

      It should be mentioned that neuronal immaturity, characteristic of the first years of human development, it is particularly sensitive to different environmental agents which can generate harmful changes in synaptic connections. Among these agents is ethanol, but it is not the only one, and in addition it can come from different emitters, often outside the pregnancy itself or the child itself.

      Some harmful effects of alcohol on Cebrero

      According to Suzanne M. Mountain and Jillian J. Kril (2014), the causes of brain degeneration and atrophy in people with alcoholism it is continuously debated in the scientific community.

      In their review of Human Alcohol-Related Neuropathology, published in the journal Acta Neuropathologica, we are told that the main tissues that affect the mature brain from prolonged alcohol consumption are: Purkinje cells and granular fibers and white matter. We will briefly explain what the above consists of.

      1. Decrease in white matter

      The most visible and studied harmful reaction in the brains of people who have consumed excess alcohol is a decrease in white matter. The resulting clinical manifestations range from subtle or undetectable deterioration to cognitive wear and tear with significant deficits in executive functions. Scientific findings suggest that cortical atrophy caused by excessive alcohol consumption is associated with permanent loss of the synapse or significant damage to its functions.

        2. Granule cells and Purkinje cells

        Granule cells are the smallest in the brain. They are found in different parts of the cerebellum, bordering the Purkinje cells, which are a type of neuron known as GABAergic. These are among the largest neurons located to date.

        Among other things, they are responsible for the regulation of sensory and motor functions. Regular alcohol consumption for 20 to 30 years produces a 15% reduction in Purkinje cells, while heavy consumption in the same years produces 33.4% (from Mountain and Kril, 2014). The degeneration of these cells in the vermis (The space dividing the two cerebral hemispheres) correlates with the development of ataxia; while its loss in the side lobes has been linked to cognitive impairment.

        to summarize

        In short, we can say that alcohol it can cause temporary and permanent deterioration in the activity of nerve cells, the product of important changes in the structure of these cells and their ability to establish communication.

        To a large extent, the severity of deterioration depends on the length of exposure to alcohol, as well as on age. the person and the specific area of ​​the brain where the disease has occurred.

        If the damage is permanent, it is neuronal death, but this has only been studied in the case of people’s ethanol consumption is not just recreational, but excessive and prolonged. The programmed loss of neuronal activity has also been studied by exposure to alcohol during the perinatal period and in organisms with few years of life.

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

        Bibliographical references:

        • De la Monte, S. and Kril, J. (2014). Human neuropathology related to alcohol. Acta Neuropathologica, 127: 71-90.
        • Creeley, C. and Olney, J. (2013). Drug-induced apoptosis: The mechanism by which alcohol and many other drugs can affect brain development. Brain Sciences, 3: 1153-1181.
        • Tokuda, K., Izumi, Y., Zorumski, CF. (2011). Ethanol enhances neurosteroidogenesis in pyramidal neurons of the hippocampus by paradoxical activation of the NMDA receptor. Journal of Neuroscience, 31 (27): 1660-11.
        • Feldstein, A. and Gores, G. (2005). Apoptosis in alcoholic and non-alcoholic steatohepatitis. Frontiers in Bioscience, 10: 3093-3099.
        • Ell, J., Nixon, K., Shetty, A. and 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 perspectives and new problems in developmental neurotoxicology. NeuroToxicology, 23 (6): 659-668.
        • Goodlett, C. and Horn, K. (2001). Mechanisms of alcohol damage to the developing nervous system. Alcohol and health research. 25 (3): 175-184.
        • Sánchez, V. (2001). Mechanisms regulating non-necrotic cell death. Cuban Journal of Biomedical Research, 20 (4): 266-274.

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