A recent finding from the COGA project has found a genetic linkage (within families) and linkage disequilibrium (across families) between the beta frequency of the EEG and a GABAA receptor gene (i.e., they co-occur at a higher frequency than would be predicted by chance) (Porjesz et al. 2002). Furthermore, several neuroimaging studies of alcoholics have shown deficits in the GABA receptors for the chemical benzodiazepine, which facilitates inhibitory GABAergic transmission (Abi-Dargham et al. 1998; Lingford-Hughes et al. 1998). Researchers also have reported neuronal loss or shrinkage in the superior frontal and motor cortices of alcoholics (Harper and Kril 1993). Taken together, these findings suggest that this deficit in GABA receptors in the brains of alcoholics may account for their lack of CNS inhibition (i.e., hyperexcitability). Recent findings from the COGA project indicate that the same GABAA receptor gene associated with the beta frequency of the EEG also is associated with a diagnosis of alcohol dependence, based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM–IV) (Edenberg et al. 2004). This suggests that variations in the
