Neurobiological mechanisms underlying the cognitive deficits associated with the nicotine withdrawal syndrome

Identifier:  TFG:106

Handle: https://hdl.handle.net/20.500.11797/TFG106

Authors:  Rodriguez Garcia, Anna

Abstract:
Tobacco use is a major public health challenge that leads to millions of preventable deaths every year. Despite this, tobacco consumption is common throughout the world. Near 80% smokers attempting to quit will relapse within the first month of abstinence. Smoking cessation produces unpleasant physiological, affective, and cognitive withdrawal symptoms that peak within the first days of nicotine deprivation. It has been suggested that relapse after smoking cessation may occur to ameliorate the cognitive impairment because nicotine re-exposure reverses this cognitive deficit. In addition, poor cognitive performance during nicotine abstinence predicted more rapid smoking resumption in the first days of abstinence. These data support the idea that the existence of cognitive deficits during nicotine withdrawal could be an important factor in the relapse of tobacco consumption. Our main objective was to investigate the possible neurobiological mechanisms involved in the nicotine-withdrawal memory impairment. We identify the endocannabinoid system as important targets associated with the memory impairment related to the nicotine withdrawal syndrome.