Elevated plasma level of apolipoprotein D in schizophrenia and its treatment and outcome.

Elevated plasma level of apolipoprotein D in schizophrenia and its treatment and outcome.
复制标题

精神分裂症中载脂蛋白 D 血浆水平升高及其治疗和结果。

DOI:
10.1016/s0920-9964(01)00378-4
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发表时间:
2002
影响因子:
4.5
通讯作者:
Parikh,VinayV
Parikh,VinayV
中科院分区:
医学2区
文献类型:
--
作者:
Mahadik,SahebaraoP;Khan,MohammadM;Evans,DeniseR;Parikh,VinayV

文献摘要

相似文献

最近,载脂蛋白D(apoD),一种参与必需多不饱和脂肪酸(EPUFA)的运输和代谢,以及神经元的生长和再生的蛋白质被报道在精神分裂症患者死后的大脑中增加,而在血清中减少。我们研究了血浆载脂蛋白D水平在精神病发作时从未服药的精神分裂症患者和慢性患者与氯氮平治疗。血浆apoD水平升高,从未服药的患者在精神病首次发作相比,正常人(P=0.047)。有趣的是,与正常人和首次发作患者相比,氯氮平治疗的慢性患者apoD水平的增加更为显著(分别为P=0.008和P=0.03)。首次发作患者从未接受过药物治疗,apoD水平升高表明,这种升高可能早于疾病,因为疾病持续时间<5天。类似地,氯氮平治疗后apoD的更大增加可能与其预防作用相关,因为精神病理学评分显著降低,并且已发现氯氮平治疗可增加EPUFA膜水平。这些改变的apoD水平可能有助于理解精神分裂症磷脂膜病理的性质和可能的机制。
Recently, apolipoprotein D (apoD), a protein that is involved in the essential polyunsaturated fatty acid (EPUFA) transport and metabolism, and neuronal growth and regeneration was reported to have increased in the postmortem brain and decreased in the serum of schizophrenia patients. We studied the plasma apoD levels in never-medicated schizophrenic patients at the onset of psychosis and in chronic patients with clozapine treatment. Plasma apoD levels were elevated in never-medicated patients at the first-episode of psychosis compared to normals (P=0.047). Interestingly, the increase in apoD level was even more significant in chronic patients treated with clozapine compared to normals and first-episode patients (P=0.008 and P=0.03, respectively). The increased apoD level in never-medicated first-episode patients indicate that this increase probably predates the illness, since the duration of illness was <5 days. Similarly, an even larger increase in apoD after clozapine treatment may be associated with its prophylactic effects, since the psychopathological scores were significantly reduced and the clozapine treatment has been found to increase the EPUFA membrane levels. These altered levels of apoD may help to understand the nature and possible mechanism of phospholipid membrane pathology in schizophrenia.