Formaldehyde initiates memory and motor impairments under weightlessness condition.

IF 4.4 1区 物理与天体物理 Q1 MULTIDISCIPLINARY SCIENCES npj Microgravity Pub Date : 2024-10-28 DOI:10.1038/s41526-024-00441-0
Tianhao Mei, Ying Chen, Yajuan Gao, Hang Zhao, Xingzhou Lyu, Jing Lin, Tianye Niu, Hongbin Han, Zhiqian Tong
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Abstract

During space flight, prolonged weightlessness stress exerts a range of detrimental impacts on the physiology and psychology of astronauts. These manifestations encompass depressive symptoms, anxiety, and impairments in both short-term memory and motor functions, albeit the precise underlying mechanisms remain elusive. Recent studies have revealed that hindlimb unloading (HU) animal models, which simulate space weightlessness, exhibited a disorder in memory and motor function associated with endogenous formaldehyde (FA) accumulation in the hippocampus and cerebellum, disruption of brain extracellular space (ECS), and blockage of interstitial fluid (ISF) drainage. Notably, the impairment of the blood-brain barrier (BBB) caused by space weightlessness elicits the infiltration of albumin and hemoglobin from the blood vessels into the brain ECS. However, excessive FA has the potential to form cross-links between these two proteins and amyloid-beta (Aβ), thereby obstructing ECS and inducing neuron death. Moreover, FA can inhibit N-methyl-D-aspartate (NMDA) currents by crosslinking NR1 and NR2B subunits, thus impairing memory. Additionally, FA has the ability to modulate the levels of certain microRNAs (miRNAs) such as miRNA-29b, which can affect the expression of aquaporin-4 (AQP4) so as to regulate ECS structure and ISF drainage. Especially, the accumulation of FA may inactivate the ataxia telangiectasia-mutated (ATM) protein kinase by forming cross-linking, a process that is associated with ataxia. Hence, this review presents that weightlessness stress-derived FA may potentially serve as a crucial catalyst in the deterioration of memory and motor abilities in the context of microgravity.

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甲醛会导致失重状态下的记忆和运动障碍。
在太空飞行期间,长时间的失重压力会对宇航员的生理和心理产生一系列不利影响。这些表现包括抑郁症状、焦虑以及短期记忆和运动功能受损,但其确切的内在机制仍然难以捉摸。最近的研究发现,模拟太空失重的后肢卸载(HU)动物模型表现出记忆和运动功能紊乱,这与海马和小脑内源性甲醛(FA)积累、脑细胞外空间(ECS)破坏和间质(ISF)引流受阻有关。值得注意的是,太空失重导致血脑屏障(BBB)受损,引起血管中的白蛋白和血红蛋白渗入脑细胞外空间。然而,过量的 FA 有可能在这两种蛋白质和淀粉样β(Aβ)之间形成交联,从而阻碍 ECS 并导致神经元死亡。此外,FA 还能通过交联 NR1 和 NR2B 亚基抑制 N-甲基-D-天冬氨酸(NMDA)电流,从而损害记忆。此外,FA 还能调节某些微小核糖核酸(miRNA)(如 miRNA-29b)的水平,而 miRNA-29b 可影响水通道蛋白-4(AQP4)的表达,从而调节 ECS 结构和 ISF 排泄。特别是,FA 的积累可能通过形成交联而使共济失调性毛细血管扩张症(ATM)蛋白激酶失活,这一过程与共济失调有关。因此,本综述认为,失重应激产生的 FA 有可能成为微重力环境下记忆和运动能力退化的关键催化剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
npj Microgravity
npj Microgravity Physics and Astronomy-Physics and Astronomy (miscellaneous)
CiteScore
7.30
自引率
7.80%
发文量
50
审稿时长
9 weeks
期刊介绍: A new open access, online-only, multidisciplinary research journal, npj Microgravity is dedicated to publishing the most important scientific advances in the life sciences, physical sciences, and engineering fields that are facilitated by spaceflight and analogue platforms.
期刊最新文献
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