CD33/TREM2 Signaling Mediates Sleep Deprivation-Induced Memory Impairment by Regulating Microglial Phagocytosis

Tan, Shuwen; Gao, Hui; Sun, Jing; Li, Na; Zhang, Yuxin; Liu, Yang; Wang, Min; Wang, Qiang; Zhai, Qian

doi:10.1007/s12017-023-08733-6

Cited by 8 publications

(4 citation statements)

References 58 publications

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“…In regards to microglia, our morphometric analysis aligns with the inflammatory profile described in previous studies [ 58 , 59 ] (reviewed in [ 48 , 60 ]). This transformational profile is associated with increased phagocytic index [ 61 , 62 ], greater production of pro-inflammatory cytokines [ 63 ], alteration of synaptic pruning patterns [ 64 ], and neuronal apoptosis [ 65 ]. While our data seems to match these phenomena, we should mention that some authors have proposed that, chronically activated microglial cells shift to an anti-inflammatory state that improves survival rates of the remaining cells after injury [ 66 ] (reviewed in [ 67 ]).…”

Section: Discussionmentioning

confidence: 99%

Acoustic Stress Induces Opposite Proliferative/Transformative Effects in Hippocampal Glia

Cruz-Mendoza

Luquı́n

Garcı́a-Estrada

et al. 2023

IJMS

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The hippocampus is a brain region crucially involved in regulating stress responses and highly sensitive to environmental changes, with elevated proliferative and adaptive activity of neurons and glial cells. Despite the prevalence of environmental noise as a stressor, its effects on hippocampal cytoarchitecture remain largely unknown. In this study, we aimed to investigate the impact of acoustic stress on hippocampal proliferation and glial cytoarchitecture in adult male rats, using environmental noise as a stress model. After 21 days of noise exposure, our results showed abnormal cellular proliferation in the hippocampus, with an inverse effect on the proliferation ratios of astrocytes and microglia. Both cell lineages also displayed atrophic morphologies with fewer processes and lower densities in the noise-stressed animals. Our findings suggest that, stress not only affects neurogenesis and neuronal death in the hippocampus, but also the proliferation ratio, cell density, and morphology of glial cells, potentially triggering an inflammatory-like response that compromises their homeostatic and repair functions.

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Section: Discussionmentioning

confidence: 99%

Acoustic Stress Induces Opposite Proliferative/Transformative Effects in Hippocampal Glia

Cruz-Mendoza

Luquı́n

Garcı́a-Estrada

et al. 2023

IJMS

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“…Besides, many studies have begun to pay attention to cholesterol metabolism in microglia [46,47], and our previous study has revealed that microglial activation is excessively enhanced in the CSR mice [7].…”

Section: Discussionmentioning

confidence: 99%

“…It is worth noting that synaptic plasticity is critical for learning and memory [6]. A recent study showed that defective working memory with decreased synaptic density and dendritic spines was detected in sleep-deprived mice [7]. Therefore, there is strong evidence demonstrating that synaptic plasticity is closely related to the recovery and improvement of cognitive impairment after chronic sleep restriction (CSR).…”

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confidence: 99%

Trimethylamine N-oxide / SREBP2 pathway is involved in sleep deprivation-induced cognitive dysfunction through regulating astrocytic cholesterol metabolism

Zhu,

Wang,

et al. 2023

Preprint

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Sleep deprivation (SD) contributes to cognitive impairment. Astrocytic cholesterol biosynthesis is crucial for brain cholesterol homeostasis and cognitive function. However, the underlying mechanism of astrocytic cholesterol metabolism in SD-induced cognitive impairment has not been fully explored. Trimethylamine N-oxide (TMAO), a product of liver flavin-containing monooxygenase-3 (FMO3), has been shown to be increased in the urine of sleep-deprived humans and implicated with peripheral cholesterol metabolism. Nevertheless, how TMAO affects brain cholesterol metabolism remains unclear. In our study, increased FMO3 and brain TMAO levels were observed in the SD mice and elevated levels of TMAO were confirmed to lead to SD-induced cognitive dysfunction. In addition, we found that the expression of sterol regulatory element-binding protein 2 (SREBP2) is decreased in the brain of SD mice, resulting in the reduction in brain cholesterol synthesis, which in turn causes synaptic damage. Moreover, we demonstrated that TMAO inhibits the expression of SREBP2 by direct action. In contrast, FMO3 inhibitor 3,3'-diindolylmethane (DIM) alleviates SD-induced cognitive impairment by targeting the liver-brain axis. In conclusion, our study revealed that TMAO / SREBP2 pathway is involved in memory impairment in SD mice through deregulating astrocytic cholesterol metabolism.

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“…Microglia are found to be crucial for protecting fear-conditioning memories formed during the recovery sleep after a period of SD [ 110 ]. SD-induced memory impairment by regulating microglial phagocytosis is accomplished by CD33/TREM2 signaling [ 111 ]. SD induces spatial memory impairment in rats through altered neuroinflammatory responses and glial cell activation in the hippocampus [ 57 ].…”

Section: Potentially Relevant Mechanismsmentioning

confidence: 99%

The Devastating Effects of Sleep Deprivation on Memory: Lessons from Rodent Models

et al. 2023

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In this narrative review article, we discuss the role of sleep deprivation (SD) in memory processing in rodent models. Numerous studies have examined the effects of SD on memory, with the majority showing that sleep disorders negatively affect memory. Currently, a consensus has not been established on which damage mechanism is the most appropriate. This critical issue in the neuroscience of sleep remains largely unknown. This review article aims to elucidate the mechanisms that underlie the damaging effects of SD on memory. It also proposes a scientific solution that might explain some findings. We have chosen to summarize literature that is both representative and comprehensive, as well as innovative in its approach. We examined the effects of SD on memory, including synaptic plasticity, neuritis, oxidative stress, and neurotransmitters. Results provide valuable insights into the mechanisms by which SD impairs memory function.

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CD33/TREM2 Signaling Mediates Sleep Deprivation-Induced Memory Impairment by Regulating Microglial Phagocytosis

Cited by 8 publications

References 58 publications

Acoustic Stress Induces Opposite Proliferative/Transformative Effects in Hippocampal Glia

Acoustic Stress Induces Opposite Proliferative/Transformative Effects in Hippocampal Glia

Trimethylamine N-oxide / SREBP2 pathway is involved in sleep deprivation-induced cognitive dysfunction through regulating astrocytic cholesterol metabolism

The Devastating Effects of Sleep Deprivation on Memory: Lessons from Rodent Models

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