摘要

Studies in alcohol-dependent patients show that cognitive function can be influenced by chronic use of alcohol. Alcohol is a known neurotoxin that induces neurodegeneration in the brain. Although there are various causes of cognitive deficiency in alcohol-dependent patients, in this study we focus on the role of corticosteroids. The hypothalamus-pituitary-adrenal system (i.e., the HPA axis) plays a part in the control of corticosteroids. Recent studies show that insulin-like growth factor-1 (IGF-1) reflects the status of growth hormones under the action of the 1-HPA axis. Therefore, IGF-1 is a potential indicator that reflects activity of the 1-IPA axis, and a biomarker that may reflect the decline of cognitive function associated with alcohol-induced hypercortisolism. The purposes of this study are to identify an association between cognitive function and IGF-1, and to investigate IGF as the biological marker of cognitive decline in alcoholdependent patients. Forty alcohol-dependent patients were selected as the subjects of this study. IGF-1 was measured through an enzyme-linked immunosorbent assay (ELISA). Clinical features were examined using the Korean version of the alcohol dependence scale (ADS-K). Cognitive functions were measured using the Consortium to Establish a Registry for Alzheimer%26apos;s Disease (CERAD). Comparative analysis was utilized to identify an association between CERAD measurement items and IGF-1. Alcohol-dependent patients demonstrated stable performance of most of the CERAD measures. Among the measures of the CERAD, only trail making test A showed a correlation to IGF-1. Compared to trail making test B, trail making test A is assumed to reflect basic cognitive functions including psychomotor speed, visual search and sequencing in alcohol-dependent patients, regardless of demographic characteristics such as the level of education of patients. Therefore, IGF-1 seems to play an important role in detecting the decline of basic cognitive functions in alcohol-dependent patients.

  • 出版日期2014-11-7