COMT genotype predicts longitudinal cognitive decline and psychosis in 22q11.2 deletion syndrome

被引:255
作者
Gothelf, D
Eliez, S
Thompson, T
Hinard, C
Penniman, L
Feinstein, C
Kwon, H
Jin, ST
Jo, B
Antonarakis, SE
Morris, MA
Reiss, AL
机构
[1] Stanford Univ, Sch Med, Ctr Interdisciplinary Brain Sci Res, Stanford, CA 94305 USA
[2] Tel Aviv Univ, Sackler Fac Med, Ramat Aviv, Israel
[3] Univ Geneva, Sch Med, Dept Psychiat, CH-1206 Geneva, Switzerland
[4] Univ Hosp Geneva, Med Genet Serv, CH-1211 Geneva, Switzerland
[5] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98104 USA
[6] Ctr Med Univ Geneva, Univ Med Sch, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland
关键词
D O I
10.1038/nn1572
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Although schizophrenia is strongly hereditary, there are limited data regarding biological risk factors and pathophysiological processes. In this longitudinal study of adolescents with 22q11.2 deletion syndrome, we identified the catechol-O-methyltransferase low-activity allele (COMTL) as a risk factor for decline in prefrontal cortical volume and cognition, as well as for the consequent development of psychotic symptoms during adolescence. The 22q11.2 deletion syndrome is a promising model for identifying biomarkers related to the development of schizophrenia.
引用
收藏
页码:1500 / 1502
页数:3
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