There is also a genetic risk for proinflammatory cytokine mediated alcohol-related brain damage. There is evidence that variants of these genes are involved not only in contributing to brain damage but also to impulsivity and alcohol abuse . All three of these genetic traits contribute heavily to an alcohol use disorder. The volume of the corpus callosum, a large white matter tract that connects the two  hemispheres, is shown to decrease with alcohol abuse due to a loss of myelination. This integration between the two cerebral hemispheres and cognitive function is affected. A limited amount of myelin can be restored with alcohol abstinence, leading to transient neurological deficits. Alcohol abuse affects neurons in the frontal cortex that typically have a large soma, or cell body. This type of neuron is more susceptible to Alzheimer's disease and normal aging. Research is still being conducted to determine whether there is a direct link between excessive alcohol consumption and Alzheimer's disease. Higher order functioning of the cerebral cortex is organized by the cerebellum. In those with cerebral atrophy, Purkinje cells, or the cerebellar output neurons, in the vermis are reduced in number by 43\%. This large reduction in purkinje cells causes a decrease in high order cerebral cortex organization. The cerebellum is also responsible for refining crude motor output from the primary motor cortex. When this refinement is missing, symptoms such as unsteadiness and ataxia will present. A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor. This dysfunction causes an increase in the neurotransmitter GABA in cerebellar purkinje cells, granule cells, and interneurons leading to a disruption in normal cell signaling. GABA-A Receptor embedded in cell membrane Neuroimaging Neuroimaging is used to study the effect that alcohol has on the brain. The two main imaging methods are hemo-dynamic and electromagnetic. These techniques have allowed for the study of the functional, biochemical, and anatomical changes of the brain due to prolonged alcohol abuse . Neuroimaging provides valuable information in determining the risk an individual has for developing alcohol dependence and the efficacy of potential treatment. Hemodynamic methods record changes in blood volume, blood flow, blood oxygenation, and energy metabolism to produce images. Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) are common techniques that require the injection of a radioactively labeled molecule, such as glucose, to allow for proper visualization. After injection, the patient is then observed while performing mental tasks, such as a memory task. PET and SPECT studies have confirmed and expanded previous findings stating that the prefrontal cortex is particularly susceptible to decreased metabolism in alcohol abusing patients .
There is also a genetic risk for proinflammatory cytokine mediated alcohol-related brain damage. There is evidence that variants of these genes are involved not only in contributing to brain damage but also to impulsivity and alcohol use disorder . All three of these genetic traits contribute heavily to an alcohol use disorder. The volume of the corpus callosum, a large white matter tract that connects the two cerebral hemispheres, is shown to decrease with alcohol misuse due to a loss of myelination. This integration between the two cerebral hemispheres and cognitive function is affected. A limited amount of myelin can be restored with alcohol abstinence, leading to transient neurological deficits. Alcohol misuse affects neurons in the frontal cortex that typically have a large soma, or cell body. This type of neuron is more susceptible to Alzheimer's disease and normal aging. Research is still being conducted to determine whether there is a direct link between excessive alcohol consumption and Alzheimer's disease. Higher order functioning of the cerebral cortex is organized by the cerebellum. In those with cerebral atrophy, Purkinje cells, or the cerebellar output neurons, in the vermis are reduced in number by 43\%. This large reduction in Purkinje cells causes a decrease in high order cerebral cortex organization. The cerebellum is also responsible for refining crude motor output from the primary motor cortex. When this refinement is missing, symptoms such as unsteadiness and ataxia will present. A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor. This dysfunction causes an increase in the neurotransmitter GABA in cerebellar purkinje cells, granule cells, and interneurons leading to a disruption in normal cell signaling. GABA-A Receptor embedded in cell membrane Neuroimaging Neuroimaging is used to study the effect that alcohol has on the brain. The two main imaging methods are hemodynamic and electromagnetic. These techniques have allowed for the study of the functional, biochemical, and anatomical changes of the brain due to prolonged heavy alcohol use . Neuroimaging provides valuable information in determining the risk an individual has for developing alcohol dependence and the efficacy of potential treatment. Hemodynamic methods record changes in blood volume, blood flow, blood oxygenation, and energy metabolism to produce images. Positron emission tomography (PET) and single-photon emission computed tomography (SPECT) are common techniques that require the injection of a radioactively labeled molecule, such as glucose, to allow for proper visualization. After injection, the patient is then observed while performing mental tasks, such as a memory task. PET and SPECT studies have confirmed and expanded previous findings stating that the prefrontal cortex is particularly susceptible to decreased metabolism in people with alcohol use disorder .
R
abuse
use disorder
A
cerebral
R
abuse
misuse
R
abuse
misuse
R
purkinje
Purkinje
R
hemo-dynamic
hemodynamic
R
alcohol abuse
heavy alcohol use
R
alcohol abusing patients
people with alcohol use disorder