期刊
NATURE NEUROSCIENCE
卷 26, 期 4, 页码 587-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41593-023-01270-2
关键词
-
The authors find that 40-Hz flickering light does not suppress A beta, activate microglia or engage native gamma oscillations. Thus, visual flicker stimulation may not be a viable mechanism for altering AD pathology and modulating deep structures.
The authors find that 40-Hz flickering light does not suppress A beta, activate microglia or engage native gamma oscillations. Thus, visual flicker stimulation may not be a viable mechanism for altering AD pathology and modulating deep structures. There is a demand for noninvasive methods to ameliorate disease. We investigated whether 40-Hz flickering light entrains gamma oscillations and suppresses amyloid-beta in the brains of APP/PS1 and 5xFAD mouse models of Alzheimer's disease. We used multisite silicon probe recording in the visual cortex, entorhinal cortex or the hippocampus and found that 40-Hz flickering simulation did not engage native gamma oscillations in these regions. Additionally, spike responses in the hippocampus were weak, suggesting 40-Hz light does not effectively entrain deep structures. Mice avoided 40-Hz flickering light, associated with elevated cholinergic activity in the hippocampus. We found no reliable changes in plaque count or microglia morphology by either immunohistochemistry or in vivo two-photon imaging following 40-Hz stimulation, nor reduced levels of amyloid-beta 40/42. Thus, visual flicker stimulation may not be a viable mechanism for modulating activity in deep structures.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据