In this review the naturally occurring β-carbolines norharman and harman in human beings and mammals will be discussed. These β-carbolines have been recognized as aromatic alkaloids, which can be detected in very low concentrations in human plasma. Norharman and especially harman display moderate affinity to the benzodiazepine receptor. The biosynthesis of these compounds in vivo, the localization, the biological effects and the probable involvement of these compounds in the cause of psychopathologic states will be discussed. This with a special focus on alcoholism, heroin addiction, psychosis and anxiety disorders. In some of these clinical pictures the concentration of norharman is increased. Whether this is a causality or a matter of minor importance is still unknown.

The controversy concerning the concept ‘alcoholic dementia’ is reviewed in brief. Evidence from neuroradiological and neuropathological studies contribute little to the solution of this controversy, if dementia is considered as a clinical syndrome. From clinical descriptions it can be concluded that a sub-population of alcoholics suffers from a syndrome typified by psychologic disturbances other than amnesia alone. These patients fulfill the criteria for the syndromal diagnosis of ‘dementia’.

The nosologic concept of ‘alcoholic dementia’ implies a direct neurotoxic effect of alcohol and it raises questions concerning pathogenetic mechanisms which can not be answered. The DSM-III-R category ‘dementia associated with alcoholism’ represents a solution for this controversy, because it gives a correct and complete (radically syndromal) clinical description without making assumptions on the relative contribution of multiple factors causing cognitive disturbances in alcoholics.