Academic journal article Alcohol Research

Alcohol-Related Neurodegeneration and Recovery: Mechanisms from Animal Models

Academic journal article Alcohol Research

Alcohol-Related Neurodegeneration and Recovery: Mechanisms from Animal Models

Article excerpt

The discovery that alcoholic humans have small brains is confounded by not knowing what the brain size was before alcoholism. Smaller human alcoholic brains could be attributed to smaller brain volume increasing risk for becoming alcoholic, alcohol-induced brain shrinkage, or both. Because mammalian brains are similar, animal studies allow investigation of the brain before, during, and after alcohol intoxication, as well as investigation of other factors that complicate understanding human disease. Animal studies continue to be used to model human responses in order to understand how to better prevent and reverse human problems. One key finding from animal studies is that high blood alcohol levels which occur with binge drinking and alcoholism can cause neurodegeneration without any nutritional or other deficiency (Crews and Nixon 2008).

Neurodegeneration is defined as the loss of structure or function of brain cells, including death of neurons and other cellular components. Alcoholic neurodegeneration is subtle, widespread, and varied but can be compared with other neurodegenerative diseases (Rosenbloom and Pfefferbaum 2008). This article will review studies on animal models of alcoholism that indicate multiple mechanisms of alcohol neurodegeneration and loss of key brain functions related to addiction. Other animal studies of brain regeneration in abstinent alcohol-treated animals will be related to human studies investigating changes in the abstinent alcoholic human brain. The integration of animal experimentation with human clinical discoveries supports the significant role of alcohol abuse and abstinence following chronic alcohol abuse in changing brain structure that corresponds with changes in cognition.

ADVANTAGES OF USING ANIMAL MODELS TO STUDY ALCOHOLIC NEURODEGENERATION

Animal models can be used to clearly test hypotheses about disease factors found in humans. Humans vary in size, weight, age, genetics, diet, and behaviors, including alcohol and tobacco consumption as well as vitamin and aspirin use, exercise, and multiple environmental factors. All of these factors influence health in complex ways that are difficult to untangle when studying people. High-risk alcohol-drinking patterns, including binge drinking (i.e., five drinks for men or four drinks for women in 2 hours) and heavy drinking (i.e., five or more drinks per day for men and four or more drinks per day for women), increase health risks including risk for alcoholism. Alcoholism is a medically defined complex disease with multiple symptoms, the most prominent of which are impulsive and compulsive use of alcohol despite knowing it interferes with mental, physical, and social well-being. Common markers of alcoholism include tolerance to alcohol (i.e., the ability to drink increasingly large amounts) and withdrawal from alcohol (i.e., experiencing bad feelings, tremor, and other symptoms when not drinking). Animal studies of binge and heavy drinking, alcohol tolerance and physical dependence, and the biological effects of alcohol offer the advantage of closely controlling factors that cannot be controlled in human studies. These studies allow researchers to better understand the effects of alcohol on physical and mental health.

Human studies have found reduced gray and white matter in the brains of alcoholics compared with nonalcoholics (see Rosenbloom and Pfefferbaum in this issue, pp. 362-376). Interpreting how much of the reduction in brain size is caused by alcohol consumption may be complicated by variations in brain size among individuals and changes in brain size with age. Human brain volumes decrease with age, and this must be considered when studying the effects of alcohol on the brain (Sullivan and Pfefferbaum 2007). Patterns of drinking vary between people and over time in the same individual, complicating the study of the effect of alcohol on neurodegeneration across individuals (Rosenbloom and Pfefferbaum in this issue. …

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