Kern Janet K, Jones Anne M
Department of Psychiatry, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9119, USA.
J Toxicol Environ Health B Crit Rev. 2006 Nov-Dec;9(6):485-99. doi: 10.1080/10937400600882079.
According to the Autism Society of America, autism is now considered to be an epidemic. The increase in the rate of autism revealed by epidemiological studies and government reports implicates the importance of external or environmental factors that may be changing. This article discusses the evidence for the case that some children with autism may become autistic from neuronal cell death or brain damage sometime after birth as result of insult; and addresses the hypotheses that toxicity and oxidative stress may be a cause of neuronal insult in autism. The article first describes the Purkinje cell loss found in autism, Purkinje cell physiology and vulnerability, and the evidence for postnatal cell loss. Second, the article describes the increased brain volume in autism and how it may be related to the Purkinje cell loss. Third, the evidence for toxicity and oxidative stress is covered and the possible involvement of glutathione is discussed. Finally, the article discusses what may be happening over the course of development and the multiple factors that may interplay and make these children more vulnerable to toxicity, oxidative stress, and neuronal insult.
根据美国自闭症协会的说法，自闭症如今被视为一种流行病。流行病学研究和政府报告所揭示的自闭症发病率上升，暗示了可能正在发生变化的外部或环境因素的重要性。本文讨论了一些自闭症儿童可能因出生后某个时候受到损伤导致神经元细胞死亡或脑损伤而患上自闭症这一情况的证据；并探讨了毒性和氧化应激可能是自闭症中神经元损伤原因的假说。文章首先描述了在自闭症中发现的浦肯野细胞丢失、浦肯野细胞生理学和易损性，以及出生后细胞丢失的证据。其次，文章描述了自闭症中脑容量增加的情况以及它可能与浦肯野细胞丢失的关系。第三，涵盖了毒性和氧化应激的证据，并讨论了谷胱甘肽可能的参与情况。最后，文章讨论了在发育过程中可能发生的情况以及可能相互作用并使这些儿童更容易受到毒性、氧化应激和神经元损伤影响的多种因素。
