Alcohol is a lipophilic substance, and it is easy to enter the brain through the blood-brain barrier. The organs of the human body that contain the highest amount of fat are neural tissues, and the brain is in the first place, especially the cerebral cortex and reticular structures are the most sensitive. Generally speaking, adults who drink more than 250 ML of liquor daily for 10-20 years can develop chronic alcoholism, and brain atrophy is almost universally seen in chronic alcoholism. Similarly, alcohol can directly damage the cerebral cortex and subcortical areas, causing dehydration, degeneration, and necrosis of brain cells, resulting in cellular atrophy of nerve cells and causing increased cerebral capillary resistance, decreased blood flow, and occlusion of small deep arteries. The brain eventually produces functional and morphological changes under long-term ischemia and hypoxia, resulting in diffuse cerebral atrophy. Autopsies of patients who died of chronic alcoholism revealed reduced brain weight, cortical atrophy, enlarged perirhinal space, enlarged ventricles and reduced white matter volume, and microscopic findings of atrophy and loss of cortical nerve cells and reduced axons and dendrites of nerve cells. In addition, in patients with chronic alcoholism, there is increased water content and decreased lipids in the white matter of the brain, and there are pathological changes such as gliosis, edema, and demyelination. The prevalence of brain atrophy has been reported to be significantly higher in the brain atrophy group than in the control group. The aging and death of nerve cells and the massive loss of gangliosides likewise lead to brain atrophy, which can also cause memory and cognitive decline. The close relationship between the severity of brain atrophy and the degree of dementia has also been demonstrated in studies related to dementia changes in patients with multiple infarct dementia.