阿里斯托斯·喬治烏文 劉偉譯

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 neurons 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.

Its important to note， however， that at present it isnt 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 Aspergers syndrome.

盡管自閉癥的確切原因不明，但目前已發(fā)現(xiàn)，兒童患上此病與各種遺傳和環(huán)境因素有關(guān)，其中包括缺鋅。

根據(jù)《分子神經(jīng)科學(xué)前言》期刊發(fā)表的論文，雖然現(xiàn)在仍不清楚缺鋅是否會(huì)導(dǎo)致自閉癥，但科學(xué)家指明了它產(chǎn)生這種影響的可能作用機(jī)制。在其研究中，研究者證明了鋅如何通過(guò)自閉癥相關(guān)基因控制的復(fù)雜分子機(jī)制，來(lái)影響早期發(fā)育過(guò)程中形成的腦細(xì)胞（神經(jīng)元）連接，或者說(shuō)突觸。

“自閉癥與特定的基因變異有關(guān)，這些基因影響早期發(fā)育過(guò)程中突觸的形成、成熟和穩(wěn)定。”該研究論文的第一作者、斯坦福大學(xué)醫(yī)學(xué)院的薩莉·金在一份聲明中如是說(shuō)。

金說(shuō)：“我們的研究結(jié)果表明，通過(guò)與這些基因編碼形成的蛋白質(zhì)相互作用，神經(jīng)元中的鋅含量會(huì)導(dǎo)致自閉癥?！?/p>

研究團(tuán)隊(duì)發(fā)現(xiàn)，突觸傳遞大腦信號(hào)時(shí)，鋅就進(jìn)入目標(biāo)神經(jīng)元，在那里將SHANK2和SHANK3這兩種蛋白質(zhì)結(jié)合起來(lái)。這些蛋白質(zhì)會(huì)導(dǎo)致突觸神經(jīng)元表面相鄰信號(hào)受體（名為α-氨基-3-羥基-5-甲基-4-異唑受體）的成分和功能發(fā)生改變。

鋅會(huì)通過(guò)SHANK蛋白質(zhì)改變發(fā)育中的突觸特性，這一研究結(jié)果表明，早期發(fā)育過(guò)程中，缺鋅會(huì)損害突觸使腦細(xì)胞能夠彼此交流的功能，可能導(dǎo)致自閉癥。

該研究論文的另一主要作者、斯坦福大學(xué)醫(yī)學(xué)院的約翰·于格納爾認(rèn)為：“了解鋅和SHANK蛋白之間的相互作用就能找到自閉癥的診斷、治療和預(yù)防措施?！?/p>

然而，需要特別注意的是，目前無(wú)法做出任何具體的結(jié)論或者開始建議兒童補(bǔ)鋅。

“當(dāng)下沒(méi)有針對(duì)孕婦或嬰幼補(bǔ)鋅對(duì)自閉癥風(fēng)險(xiǎn)影響的對(duì)照研究，所以，現(xiàn)在仍無(wú)定論?！痹撗芯空撐牡牧硪晃蛔髡摺⒌聡?guó)神經(jīng)退行性疾病中心的克雷格·加納說(shuō)，“但是同樣發(fā)表在這一‘前沿研究課題專欄中的自閉癥模型實(shí)驗(yàn)研究前景樂(lè)觀?！?/p>

鋅攝入過(guò)多會(huì)降低身體對(duì)銅的吸收，導(dǎo)致貧血和骨質(zhì)疏松。此外，缺鋅不一定意味著飲食營(yíng)養(yǎng)缺乏，比如它還可能由腸道吸收問(wèn)題所致。

加納說(shuō)：“不過(guò)，我們的研究成果提供了一種新機(jī)制來(lái)了解缺鋅（或者說(shuō)鋅在神經(jīng)元中的運(yùn)作受到干擾）何以可能導(dǎo)致自閉癥?！?/p>

自閉癥是一種終身的發(fā)育障礙，影響人們對(duì)世界的感知，以及和他人的互動(dòng)。自閉癥譜系障礙包含一系列類似的疾病，比如阿斯佩格綜合征。

1 the jury is （still） out on sth〈俚語(yǔ)〉（某事）仍未定奪，懸而未決。