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While the exact cause of autism is unknown， its development in children has been linked to various genetic and environmental factors—including zinc deficiency.
It is still not clear whether this deficiency contributes to autism， but scientists have defined a possible mechanism for how this could work， according to a paper published in Frontiers in Molecular Neuroscience. For their study， the researchers demonstrated how zinc shapes the connections， or synapses， between brain cells （neurons） that form during early development via a complex molecular machinery controlled by autism-linked genes.
“Autism is associated with specific variants of genes involved in the formation， maturation and stabilization of synapses during early development，” Sally Kim， lead author of the study from Stanford University School of Medicine， said in a statement.
“Our findings link zinc levels in neurons—via interactions with the proteins encoded by these genes—to the development of autism，” Kim said.
The team found that when a brain signal was transferred via a synapse， zinc entered the target neuron where it could bind two of these proteins， known as SHANK2 and SHANK3. Those proteins cause changes in the composition and function of adjacent signal receptors， called AMPARs， on the neuron’s surface at the synapse.
The finding that zinc shapes the properties of developing synapses via SHANK proteins suggests that a lack of the mineral during early development could potentially contribute to autism by impairing the function of synapses， which enable brain cells to communicate with one another.
“Understanding the interaction between zinc and SHANK proteins could therefore lead to diagnostic， treatment and prevention strategies for autism，” suggested John Huguenard， co-senior author of the study， of Stanford University School of Medicine.
It’s important to note， however， that at present it isn’t possible to make any concrete conclusions or begin recommending that children take zinc supplements.
“Currently there are no controlled studies of autism risk with zinc supplementation in pregnant women or babies， so the jury is still out1，” Craig Garner， co-author of the study from the German Centre for Neurodegenerative Diseases， said. “But experimental work in autism models also published in this Frontiers Research Topic holds promise.”
Taking too much zinc can reduce the amount of copper the body absorbs， which can result in anemia and weakening of bones. Furthermore， zinc deficiency does not necessarily imply a dietary deficiency， and could be caused by problems with absorption in the gut， for example. “Nevertheless， our findings offer a novel mechanism for understanding how zinc deficiency—or disrupted handling of zinc in neurons—might contribute to autism，” Garner said.
Autism is a lifelong developmental disability that affects how people perceive the world and interact with others. The autism spectrum contains a range of similar disorders， such as Asperger’s syndrome.
尽管自闭症的确切原因不明，但目前已发现，儿童患上此病与各种遗传和环境因素有关，其中包括缺锌。
根据《分子神经科学前言》期刊发表的论文，虽然现在仍不清楚缺锌是否会导致自闭症，但科学家指明了它产生这种影响的可能作用机制。在其研究中，研究者证明了锌如何通过自闭症相关基因控制的复杂分子机制，来影响早期发育过程中形成的脑细胞（神经元）连接，或者说突触。
“自闭症与特定的基因变异有关，这些基因影响早期发育过程中突触的形成、成熟和稳定。”该研究论文的第一作者、斯坦福大学医学院的萨莉·金在一份声明中如是说。
金说：“我们的研究结果表明，通过与这些基因编码形成的蛋白质相互作用，神经元中的锌含量会导致自闭症。”
研究团队发现，突触传递大脑信号时，锌就进入目标神经元，在那里将SHANK2和SHANK3这两种蛋白质结合起来。这些蛋白质会导致突触神经元表面相邻信号受体（名为α-氨基-3-羟基-5-甲基-4-异唑受体）的成分和功能发生改变。
锌会通过SHANK蛋白质改变发育中的突触特性，这一研究结果表明，早期发育过程中，缺锌会损害突触使脑细胞能够彼此交流的功能，可能导致自闭症。
该研究论文的另一主要作者、斯坦福大学医学院的约翰·于格纳尔认为：“了解锌和SHANK蛋白之间的相互作用就能找到自闭症的诊断、治疗和预防措施。”
然而，需要特别注意的是，目前无法做出任何具体的结论或者开始建议儿童补锌。
“当下没有针对孕妇或婴幼补锌对自闭症风险影响的对照研究，所以，现在仍无定论。”该研究论文的另一位作者、德国神经退行性疾病中心的克雷格·加纳说，“但是同样发表在这一‘前沿研究课题’专栏中的自闭症模型实验研究前景乐观。”
鋅摄入过多会降低身体对铜的吸收，导致贫血和骨质疏松。此外，缺锌不一定意味着饮食营养缺乏，比如它还可能由肠道吸收问题所致。
加纳说：“不过，我们的研究成果提供了一种新机制来了解缺锌（或者说锌在神经元中的运作受到干扰）何以可能导致自闭症。”
自闭症是一种终身的发育障碍，影响人们对世界的感知，以及和他人的互动。自闭症谱系障碍包含一系列类似的疾病，比如阿斯佩格综合征。
1 the jury is （still） out on sth〈俚语〉（某事）仍未定夺，悬而未决。
It is still not clear whether this deficiency contributes to autism， but scientists have defined a possible mechanism for how this could work， according to a paper published in Frontiers in Molecular Neuroscience. For their study， the researchers demonstrated how zinc shapes the connections， or synapses， between brain cells （neurons） that form during early development via a complex molecular machinery controlled by autism-linked genes.
“Autism is associated with specific variants of genes involved in the formation， maturation and stabilization of synapses during early development，” Sally Kim， lead author of the study from Stanford University School of Medicine， said in a statement.
“Our findings link zinc levels in neurons—via interactions with the proteins encoded by these genes—to the development of autism，” Kim said.
The team found that when a brain signal was transferred via a synapse， zinc entered the target neuron where it could bind two of these proteins， known as SHANK2 and SHANK3. Those proteins cause changes in the composition and function of adjacent signal receptors， called AMPARs， on the neuron’s surface at the synapse.
The finding that zinc shapes the properties of developing synapses via SHANK proteins suggests that a lack of the mineral during early development could potentially contribute to autism by impairing the function of synapses， which enable brain cells to communicate with one another.
“Understanding the interaction between zinc and SHANK proteins could therefore lead to diagnostic， treatment and prevention strategies for autism，” suggested John Huguenard， co-senior author of the study， of Stanford University School of Medicine.
It’s important to note， however， that at present it isn’t possible to make any concrete conclusions or begin recommending that children take zinc supplements.
“Currently there are no controlled studies of autism risk with zinc supplementation in pregnant women or babies， so the jury is still out1，” Craig Garner， co-author of the study from the German Centre for Neurodegenerative Diseases， said. “But experimental work in autism models also published in this Frontiers Research Topic holds promise.”
Taking too much zinc can reduce the amount of copper the body absorbs， which can result in anemia and weakening of bones. Furthermore， zinc deficiency does not necessarily imply a dietary deficiency， and could be caused by problems with absorption in the gut， for example. “Nevertheless， our findings offer a novel mechanism for understanding how zinc deficiency—or disrupted handling of zinc in neurons—might contribute to autism，” Garner said.
Autism is a lifelong developmental disability that affects how people perceive the world and interact with others. The autism spectrum contains a range of similar disorders， such as Asperger’s syndrome.
尽管自闭症的确切原因不明，但目前已发现，儿童患上此病与各种遗传和环境因素有关，其中包括缺锌。
根据《分子神经科学前言》期刊发表的论文，虽然现在仍不清楚缺锌是否会导致自闭症，但科学家指明了它产生这种影响的可能作用机制。在其研究中，研究者证明了锌如何通过自闭症相关基因控制的复杂分子机制，来影响早期发育过程中形成的脑细胞（神经元）连接，或者说突触。
“自闭症与特定的基因变异有关，这些基因影响早期发育过程中突触的形成、成熟和稳定。”该研究论文的第一作者、斯坦福大学医学院的萨莉·金在一份声明中如是说。
金说：“我们的研究结果表明，通过与这些基因编码形成的蛋白质相互作用，神经元中的锌含量会导致自闭症。”
研究团队发现，突触传递大脑信号时，锌就进入目标神经元，在那里将SHANK2和SHANK3这两种蛋白质结合起来。这些蛋白质会导致突触神经元表面相邻信号受体（名为α-氨基-3-羟基-5-甲基-4-异唑受体）的成分和功能发生改变。
锌会通过SHANK蛋白质改变发育中的突触特性，这一研究结果表明，早期发育过程中，缺锌会损害突触使脑细胞能够彼此交流的功能，可能导致自闭症。
该研究论文的另一主要作者、斯坦福大学医学院的约翰·于格纳尔认为：“了解锌和SHANK蛋白之间的相互作用就能找到自闭症的诊断、治疗和预防措施。”
然而，需要特别注意的是，目前无法做出任何具体的结论或者开始建议儿童补锌。
“当下没有针对孕妇或婴幼补锌对自闭症风险影响的对照研究，所以，现在仍无定论。”该研究论文的另一位作者、德国神经退行性疾病中心的克雷格·加纳说，“但是同样发表在这一‘前沿研究课题’专栏中的自闭症模型实验研究前景乐观。”
鋅摄入过多会降低身体对铜的吸收，导致贫血和骨质疏松。此外，缺锌不一定意味着饮食营养缺乏，比如它还可能由肠道吸收问题所致。
加纳说：“不过，我们的研究成果提供了一种新机制来了解缺锌（或者说锌在神经元中的运作受到干扰）何以可能导致自闭症。”
自闭症是一种终身的发育障碍，影响人们对世界的感知，以及和他人的互动。自闭症谱系障碍包含一系列类似的疾病，比如阿斯佩格综合征。
1 the jury is （still） out on sth〈俚语〉（某事）仍未定夺，悬而未决。