A PRELIMINARY P-31 MRS STUDY OF AUTISM - EVIDENCE FOR UNDERSYNTHESIS AND INCREASED DEGRADATION OF BRAIN MEMBRANES

被引:136
作者
MINSHEW, NJ
GOLDSTEIN, G
DOMBROWSKI, SM
PANCHALINGAM, K
PETTEGREW, JW
机构
[1] WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,AUTISM RES PROJECT,PITTSBURGH,PA 15261
[2] WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,NEUROPHYS LAB,PITTSBURGH,PA 15261
[3] HIGHLAND DR VET ADM MED CTR,PITTSBURGH,PA
关键词
AUTISM; NMR; SPECTROSCOPY; BRAIN METABOLISM; MEMBRANES;
D O I
10.1016/0006-3223(93)90017-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In this pilot study, brain high energy phosphate and membrane phospholipid metabolism were investigated in the dorsal prefrontal cortex of 11 high-functioning autistic adolescent and young adult men (the age range is 12-36 years) and 11 age-, gender-, IQ, race- and socio-economic status-matched normal controls using in vivo P-31 nuclear magnetic resonance spectroscopy (MRS). The autistic group had decreased levels of phosphocreatine and esterified ends (alphaATP + alphaADP + dinucleotides + diphosphosugars) compared to the controls. When the metabolite levels were compared within each subject group with neuropsychologic and language test scores, a common pattern of correlations was observed across measures in the autistic group, but not in the control group. As test performance declined in the autistic subjects, levels of the most labile high energy phosphate compound and of membrane building blocks decreased, and levels of membrane breakdown products increased. No significant correlations were present with age in either group or with IQ in the control group, suggesting that these findings were not the consequence of age or IQ effects. This pilot study provides tentative evidence of alterations in brain energy and phospholipid metabolism in autism that correlate with the neuropsychologic and language deficits. The findings are consistent with a hypermetabolic energy state and undersynthesis of brain membranes and may relate to the neurophysiologic and neuropathologic abnormalities in autism.
引用
收藏
页码:762 / 773
页数:12
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