This Adverse Outcome Pathway (AOP) describes the linkage between binding to proteins involved in protection against oxidative stress and impairment in learning and memory. Production, binding and degradation of Reactive Oxygen Radicals are tightly regulated in the body, and an imbalance between production and protection may cause oxidative stress, which is common to many toxicity pathways. Oxidative stress may lead to an imbalance in glutamate neurotransmission, which is involved in learning and memory. Oxidative stress may also cause cellular injury and death. During brain development and in particular during the establishment of neuronal connections and networks, such perturbations may lead to functional impairment in learning and memory. The weight-of-evidence supporting the relationship between the key events described in this AOP is based mainly on developmental effects observed after an exposure to mercury, a heavy metal known for its strong affinity to many proteins having anti-oxidant properties. This AOP is referred to as AOP 17 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).
This Adverse Outcome Pathway (AOP) describes the linkage between binding to proteins involved in protection against oxidative stress and impairment in learning and memory. Production, binding and degradation of Reactive Oxygen Radicals are tightly regulated in the body, and an imbalance between production and protection may cause oxidative stress, which is common to many toxicity pathways. Oxidative stress may lead to an imbalance in glutamate neurotransmission, which is involved in learning and memory. Oxidative stress may also cause cellular injury and death. During brain development and in particular during the establishment of neuronal connections and networks, such perturbations may lead to functional impairment in learning and memory. The weight-of-evidence supporting the relationship between the key events described in this AOP is based mainly on developmental effects observed after an exposure to mercury, a heavy metal known for its strong affinity to many proteins having anti-oxidant properties. This AOP is referred to as AOP 17 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).
可以说，人类发育中大脑变化最剧烈的两个时期是从妊娠中期到6岁和青春期。虽然产前的变化涉及增殖性神经发生和细胞凋亡，但产后的变化与其说是神经元的数量，不如说是神经元之间相互联系的数量和形式。
不良结果通路（AOP）描述了不同生物组织水平的因果关联事件的逻辑序列，该序列遵循暴露于压力源并导致对人类或野生动物的不利健康影响。AOP是成员国通过经合组织推动的毒理学知识框架的核心要素，旨在支持基于机械推理的化学风险评估。这些AOP可在AOP Wiki中获得，这是一个用于AOP开发的交互式虚拟百科全书。在制定和审查之后，认可的AOP发表在经合组织关于不良结果途径的系列文章中。随着科学知识的进步，本系列中AOP的发布并不排除对给定AOP的定期更新或新贡献。虽然AOP Wiki是一个动态工具，但只有对AOP有影响的更改才会反映在已发布AOP的后续更新中。
大脑皮层负责大量复杂的大脑功能，从感知感官刺激到警觉、记忆和语言，再到意识。哥廷根马克斯·普朗克实验医学研究所的神经生物学家解码了一种新的调节原理，该原理控制着大脑皮层复杂神经元结构的发展。
A characteristic feature of modern humans is the unusually round skull and brain, in contrast to the elongated shape seen in other human species. An interdisciplinary research team, led by the Max Planck Institutes for Psycholinguistics and Evolutionary Anthropology, brought together fossil skull data, brain imaging and genomics. By studying Neandertal DNA fragments found in the genomes of living Europeans, the scientists have now discovered genes that influence this globular shape.
