THE HYPERSEROTONEMIA OF AUTISM

THE HYPERSEROTONEMIA OF AUTISM
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DOI:
10.1111/j.1749-6632.1990.tb16893.x
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发表时间:
1990-10-15
影响因子:
5.2
通讯作者:
COHEN, DJ
COHEN, DJ
中科院分区:
综合性期刊3区
文献类型:
--
作者:
ANDERSON, GM;HORNE, WC;COHEN, DJ

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计划和正在进行的血小板功能和成分的研究应该使我们能够更好地定义我们假设存在于自闭症患者血小板中的改变。虽然大部分的研究集中在β-肾上腺素能方面,更一般的研究应该允许更好地描绘的程度的改变,并将防止过早缩小调查。方法的发展,这一直是一个必要的方面的工作,应有助于提高对血小板功能和成分的理解,以及在改善的临床工具,用于评估血小板功能的神经精神疾病和血液学。作为一个例子,在短期的体外储存条件的改善,以稳定随着时间的推移聚集和形状变化的反应被认为是必要的,可能是关键的最佳比较这些现象跨组。确定导致自闭症高血小板血症的血小板改变在几个方面都是有用的。可以预期的是,对功能改变的评估将提供一种与正常人群重叠较少的标记物,而不是血液5-HT的多测定。确定与改变的血小板有关的特定蛋白质应直接导致基因探针和染色体定位。这些,反过来,应该证明是有用的新生儿筛查,分型,更强大的遗传和家庭研究。这类工作也可能有助于早期干预和改善治疗。最后,表征的生理变化将提供一个基础,重点研究脑神经化学,以及应该建议的神经药理学干预模式。人们对自闭症高血清素血症的基本发现的信心以及从其解释中获得的潜在好处使得该领域的进一步研究引起了人们的极大兴趣。
The planned and ongoing studies of platelet function and composition should allow us to better define the alteration which we presume to be present in platelets of autistic subjects. Although much of the research focuses on serotonergic aspects, the more general research should permit a better delineation of the extent of the alteration and will protect against a premature narrowing of the inquiry. The methodological development which has been a necessary aspect of the work should contribute to an improved understanding of platelet function and composition, as well as result in improved clinical tools for the assessment of platelet functioning in neuropsychiatric disorders and hematology. As an example, improvements in short-term in vitro storage conditions to stabilize aggregation and shape change responses over time were found to be necessary, and are probably critical to an optimal comparison of these phenomena across groups. The identification of the platelet alteration which is responsible for the hyperserotonemia of autism should prove useful in several ways. It would be expected that assessment of the altered function would provide a marker with less overlap with the normal population than the multidetermined measure of blood 5-HT. Determination of the specific protein (s) involved in the altered platelet should lead directly to gene probes and chromosomal location. These, in turn, should prove useful for neonatal screening, subtyping, and more powerful genetic and family studies. Work of this sort might also allow early intervention and improved treatment. Finally, characterization of the physiological alteration would provide a basis for focusing studies of brain neurochemistry and should, as well, suggest modes of neuropharmacological intervention. The confidence that one can have in the basic finding of hyperserotonemia in autism and the potential benefits to be derived from its explication make further research in this area of great interest.