Clinical Implications of Membrane Deficits and Oxidative Stress in Schizophrenia

Of what significance are the alterations in membrane and oxidative stress? The constraint on understanding the clinical implications of these alterations are that the specific pathophysiology in schizophrenia remains unknown. However, there are several intriguing associations between clinical features of schizophrenia and the biochemical measures at issue. For example, in the prefrontal cortex, a key area implicated in schizophrenia, there is evidence for both phospholipid abnormality (e.g. Pettegrew et al., 1993) and impaired free radical metabolism (Levon et al., 1996). Since PUFA are preferentially vulnerable to free radical insult, it is conceivable that decreased membrane EFA levels also exist in these areas. Prominent negative symptoms have been associated with low levels of RBC AA levels (Glen et al., 1994) and low levels of GSH-Px (Buckman et al., 1990). Positive symptoms have been associated with low RBC AA levels (Peet et al., 1995) and correlated with SOD activity (Khan and Das, 1997). We have observed a significant correlation between positive symptoms and plasma GSH-Px (Yao et al., 1998b), and an inverse correlation between negative symptoms and SOD activity in drug-free chronic schizophrenic patients (Yao et al., 1998a). Taken together, these findings suggest that membrane deficits and oxidative stress may mediate illness expression, and further suggest the possibility of therapeutic approaches using currently available treatments (Mahadik and Evans, 1997; Reddy and Yao, 1999).

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