Aberrant accumulation of age- and disease-associated factors following neural probe implantation in a mouse model of Alzheimer's disease.

IF 3.7 3区 医学 Q2 ENGINEERING, BIOMEDICAL Journal of neural engineering Pub Date : 2023-09-01 DOI:10.1088/1741-2552/aceca5
Steven M Wellman, Olivia A Coyne, Madeline M Douglas, Takashi D Y Kozai
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Abstract

Objective. Electrical stimulation has had a profound impact on our current understanding of nervous system physiology and provided viable clinical options for addressing neurological dysfunction within the brain. Unfortunately, the brain's immune suppression of indwelling microelectrodes currently presents a major roadblock in the long-term application of neural recording and stimulating devices. In some ways, brain trauma induced by penetrating microelectrodes produces similar neuropathology as debilitating brain diseases, such as Alzheimer's disease (AD), while also suffering from end-stage neuron loss and tissue degeneration. The goal of the present study was to understand whether there may be any parallel mechanisms at play between brain injury from chronic microelectrode implantation and those of neurodegenerative disorder.Approach. We used two-photon microscopy to visualize the accumulation, if any, of age- and disease-associated factors around chronically implanted electrodes in both young and aged mouse models of AD.Main results. We determined that electrode injury leads to aberrant accumulation of lipofuscin, an age-related pigment, in wild-type and AD mice alike. Furthermore, we reveal that chronic microelectrode implantation reduces the growth of pre-existing Alzheimer's plaques while simultaneously elevating amyloid burden at the electrode-tissue interface. Lastly, we uncover novel spatial and temporal patterns of glial reactivity, axonal and myelin pathology, and neurodegeneration related to neurodegenerative disease around chronically implanted microelectrodes.Significance. This study offers multiple novel perspectives on the possible neurodegenerative mechanisms afflicting chronic brain implants, spurring new potential avenues of neuroscience investigation and design of more targeted therapies for improving neural device biocompatibility and treatment of degenerative brain disease.

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阿尔茨海默病小鼠模型植入神经探针后年龄和疾病相关因素的异常积累。
客观的电刺激对我们目前对神经系统生理学的理解产生了深远的影响,并为解决大脑中的神经功能障碍提供了可行的临床选择。不幸的是,大脑对留置微电极的免疫抑制目前是神经记录和刺激设备长期应用的主要障碍。在某些方面,穿透微电极诱导的脑损伤会产生与阿尔茨海默病(AD)等衰弱性脑疾病类似的神经病理学,同时也会导致终末期神经元丧失和组织变性。本研究的目的是了解慢性微电极植入的脑损伤和神经退行性疾病的脑损伤之间是否存在任何平行的机制。方法我们使用双光子显微镜观察了AD年轻和老年小鼠模型中长期植入电极周围年龄和疾病相关因素的积累(如果有的话)。主要结果。我们确定,电极损伤导致脂褐素(一种与年龄相关的色素)在野生型和AD小鼠中的异常积累。此外,我们发现,慢性微电极植入减少了预先存在的阿尔茨海默病斑块的生长,同时增加了电极-组织界面的淀粉样蛋白负荷。最后,我们发现了神经胶质反应性、轴突和髓鞘病理以及与神经退行性疾病相关的神经退行性变在长期植入微电极周围的新的空间和时间模式。意义这项研究为影响慢性脑植入物的可能神经退行性机制提供了多种新的视角,为神经科学研究和设计更具针对性的疗法提供了新的潜在途径,以改善神经设备的生物相容性和治疗退行性脑疾病。
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来源期刊
Journal of neural engineering
Journal of neural engineering 工程技术-工程:生物医学
CiteScore
7.80
自引率
12.50%
发文量
319
审稿时长
4.2 months
期刊介绍: The goal of Journal of Neural Engineering (JNE) is to act as a forum for the interdisciplinary field of neural engineering where neuroscientists, neurobiologists and engineers can publish their work in one periodical that bridges the gap between neuroscience and engineering. The journal publishes articles in the field of neural engineering at the molecular, cellular and systems levels. The scope of the journal encompasses experimental, computational, theoretical, clinical and applied aspects of: Innovative neurotechnology; Brain-machine (computer) interface; Neural interfacing; Bioelectronic medicines; Neuromodulation; Neural prostheses; Neural control; Neuro-rehabilitation; Neurorobotics; Optical neural engineering; Neural circuits: artificial & biological; Neuromorphic engineering; Neural tissue regeneration; Neural signal processing; Theoretical and computational neuroscience; Systems neuroscience; Translational neuroscience; Neuroimaging.
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