The GM abnormalities in schizophrenia may be, at least in part, familial/trait markers (Cannon et al., 2003; Gilbert, Montrose, Sahni, Diwadkar, & Keshavan, 2003; Weinberger & McClure, 2002; Yucel et al., 2003). Longitudinal brain MRI studies on healthy COS siblings provide further insights into the phenomenon of cortical GM changes. Longitudinal GM findings in 52 healthy full siblings of COS patients showed that these siblings had initial GM deficits which, for this group, did not progress during adolescence (unlike their COS probands) but in fact, normalized by age 20. The early GM loss in siblings was most prominent in prefrontal and temporal cortices (see Figure 4) as has been seen for COS probands, but unlike the pattern seen in probands, siblings did not show parietal GM loss at younger ages. This is also consistent with the notion that the early parietal deficits may require a non-genetic trigger, as they were absent in siblings who ultimately remained healthy. This apparent ‘plastic’ response (inhibition of cortical thinning) in healthy siblings is intriguing and warrants replication. Within the healthy sibling group, regional cortical
