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Stanford researchers develop new tool for watching and controlling neural activity
A new molecular probe from Stanford University could help reveal how our brains think and remember. This tool, called Fast Light and Calcium-Regulated Expression or FLiCRE (pronounced “flicker”), can be sent inside any cell to perform a variety of research tasks, including tagging, recording and controlling cellular functions. “This work gets at a central goal […]
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Shanghai hospital clears ethical reviews for chip brain implant treatment for depressed patients
TCCI’s recently opened Frontier Lab for Brain Research in Shanghai, is mentioned in this article which touches on progress in the area of brain-computer interfaces (BCI) in China. The article mentions that although China has been lagging in this area, recent investments in this technology, like similar work being done at the Chen Frontier Lab […]
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Hibernation: Translating Insights from Nature into Manned Deep Space Exploration
During a long‐duration manned spaceflight mission, such as flying to Mars and beyond, all crew members will spend a long period in an independent spacecraft with closed‐loop bioregenerative life‐support systems. Saving resources and reducing medical risks, particularly in mental health, are key technology gaps hampering human expedition into deep space. Professor Tifei Yuan, a Tianqiao […]
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Testing memory over four weeks could predict Alzheimer’s disease risk
New research suggests testing people’s memory over four weeks could identify who is at higher risk of developing Alzheimer’s disease before it has developed. Importantly, the trial found testing people’s ability to retain memories for longer time periods could predict this more accurately than classic memory tests, which test memory over half an hour. The […]
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Melatonin: Finally, a supplement that actually boosts memory
In a new study, researchers led by Atsuhiko Hattori at Tokyo Medical and Dental University (TMDU) in Japan have shown that melatonin and two of its metabolites help memories stick around in the brain and can shield mice, and potentially people, from cognitive decline.
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New Compound Related to Psychedelic Ibogaine Could Treat Addiction, Depression
A non-hallucinogenic version of the psychedelic drug ibogaine, with potential for treating addiction, depression and other psychiatric disorders, has been developed by researchers at the University of California, Davis. A paper describing the work is published on Dec.9th in Nature. Ibogaine is extracted from the plant Tabernanthe iboga. There are anecdotal reports that it can […]
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Memory deficits resulting from epigenetic changes in Alzheimer’s disease can be reversed
Memory loss associated with Alzheimer’s disease (AD) may be able to be restored by inhibiting certain enzymes involved in abnormal gene transcription, according to a preclinical study by researchers at the University at Buffalo. The findings could pave the way toward new treatments for Alzheimer’s disease. The paper will be published on Dec. 9 in […]
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Making Memories
Now, neuroscientists at Harvard Medical School have taken a decisive step in the quest to understand the biology of long-term memory and find ways to intervene when memory deficits occur with age or disease. Reporting in Nature on Dec. 9, they describe a newly identified mechanism that neurons in the adult mouse hippocampus use to […]
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自由基可能有益大脑健康
活性氧分子，也被称为“自由基”，一般被认为是有害的。然而，一项新研究可能得出了相反结论：在小鼠身上，它们控制着细胞过程，这对大脑的适应能力很重要。 细胞氧化还原状态调节干细胞维持和激活之间的平衡。细胞内活性氧（ROS）水平的提高与增殖和细胞谱系特异性有关。与之相反，该研究显示在成年小鼠的海马体中，静止的神经前体细胞(NPCs)维持着最高的ROS水平(hiROS)。根据细胞ROS含量对NPC进行分类可确定其不同的功能状态，ROS含量的变化引发了细胞的后续状态转换，其中较低的ROS含量标志着增殖活性和分化。身体活动是成年海马神经发生的生理激活剂，它通过短暂的Nox2依赖性ROS激增使hiROS NPC进入增殖状态，在没有Nox2的情况下，基线神经发生不受影响，但活性诱导的增殖增加却消失了。这些结果提供了NPC功能状态的代谢分类，并描述了通过行为线索将细胞ROS的调节与成年NPC的激活联系起来的机制。 研究人员表示：“过多的氧化应激是不利的，它会导致神经损伤并触发衰老过程，然而自由基也有好的一面，我们大脑中的干细胞不仅能忍受如此高水平的自由基，而且还能正常发挥它们的功能，事实上，它们对大脑在整个生命过程中保持适应性以及以健康方式衰老非常重要。”
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出生时激活的脑干多肽系统支持我们出生后的第一次呼吸
来自美国维吉尼亚大学的一个研究小组发现，出生时激活的脑干多肽系统可促进产后呼吸。 调节呼吸的神经系统在发育的早期是脆弱的，目前尚不清楚它们是如何调节以支持出生时的呼吸。在这项研究中，研究人员确定了一个神经肽系统，该系统在出生后立即被激活并支持呼吸。在梯形后核（RTN）神经元中选择性缺乏PACAP的小鼠表现出呼吸暂停增加和CO2刺激的呼吸减弱，RTN神经元中PACAP的重新表达纠正了这些呼吸不足。从pre-Bötzinger复合体（一个负责产生呼吸节律的RTN目标区域）中删除PACAP受体PAC1，显著复制了RTN缺失PACAP后观察到的呼吸不足，并抑制了pre-Bötzinger复合体中PACAP诱发的呼吸刺激。值得注意的是，恰好在出生时，RTN神经元中发生了PACAP表达的产后爆发，这与暴露于外部环境相吻合。RTN神经元中PACAP缺失的新生小鼠表现出呼吸暂停增加，环境温度的变化进一步加剧了呼吸暂停。 这些发现表明，RTN神经元适时表达的PACAP在出生后立即提供了一个重要的辅助呼吸驱动，并揭示了在生命中最为脆弱时期支持呼吸的肽能神经回路的关键分子成分。