Specificity of Biomarker for Cognitive Function in Alcoholism
The neuromolecular changes observed in cognitively impaired chronic alcoholism subjects are distinctly different from those observed in cognitively impaired schizophrenia subjects. The chronic schizophrenia figure shows those differences with p ≤ 0.01 but is otherwise as described for the alcoholism figure. Cognitively impaired chronic schizophrenia subjects (N=19 males) compared with cognitively intact chronic schizophrenia subjects (N=16 males) demonstrate decreases in membrane phospholipid building blocks [PME(s-tc)] in the right basal ganglia, and increases in measures of membrane glycosylation in the right basal ganglia and the right centrum semiovale (Pettegrew et al., 2003). These changes are distinctly different from those observed in cognitively impaired chronic alcoholism subjects.
Since many chronic alcoholism and chronic schizophrenia subjects are smokers, the neuromolecular effects of nicotine were studied. The nicotine figure shows those brain regions that have neuromolecular differences with p ≤ 0.01, but is otherwise as described for the alcoholism figure. Middle age smokers (4 males, 4 females) were examined by MRSI after receiving a nicotine or placebo patch (McClure et al., 2004). The observed nicotine effect was a decrease in membrane breakdown products [PDE(s-tc)] in the left prefrontal cortex and increases in membrane building blocks [PME(s-tc)] in the right superior temporal cortex. This pattern was not observed in the chronic alcoholism subjects, again supporting the specificity of the biomarker for cognitive impairment in chronic alcoholism.