“Olfactory Three-Needle” Enhances Spatial Learning and Memory Ability in SAMP8 Mice

Wang, Yuan; Wang, Qiang; Ren, Bo; Guo, Ting; Qiang, Jun; Cao, Hui; Gao, Yu-Jie; Liu, Zhibin; Gao, Xin-Yan; Zhu, Bing

doi:10.1155/2020/2893289

Cited by 12 publications

(9 citation statements)

References 39 publications

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“…Many previous studies have reported that the hippocampal expression of synaptophysin and PSD-95 is decreased in AD and VaD (35,36). It has also been shown that acupuncture can upregulate PSD-95 expression (37) and promote the repair of synaptic structural damage, thereby improving learning and memory in the vascular cognitive impairment mouse model (38,39). Furthermore, in 5XFAD mice, EA was shown to improve working memory and synaptic plasticity, reduce neuroinflammation, and reduce ultrastructural degradation of synapses through the upregulation of synaptophysin and PSD-95 (40).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture of the Baihui and Shenting acupoints for vascular dementia in rats through the miR-81/IL-16/PSD-95 pathway

Ma¹,

Zhou²,

Yi³

et al. 2022

Ann Transl Med

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Background: There is currently no effective treatment for vascular dementia (VaD). Scalp electroacupuncture (EA) has served clinically as an alternative treatment for VaD, but its mechanism is still unclear. In this study, we investigated the effect of EA at the Baihui (GV 20) and Shenting (GV 24) acupoints on spatial learning and memory ability, and the expression level of microRNA-81 (miR-81), interleukin-16 (IL-16), and postsynaptic density protein-95 (PSD-95) in the frontal cortex of VaD rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups, sham, VaD, nonacupuncture (non-AP) and EA group. The VaD model was established by permanent bilateral occlusion of the common carotid arteries. Morris Water Maze was used to assess the rats' spatial learning and memory.Immunochemistry (IHC), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and western blot analysis were performed to detect the expression level of miR-81, IL-16, and PSD-95. Finally, luciferase assay was used to determine the effect of miR-81 on IL-16 expression in PC12 cells. Results:The space exploration experiment of MWM showed the time and distance of the rat's activities around the platform were decreased in the EA group. Compared to the VaD and non-AP group, the number of terminal deoxynucleotidyl transferase-mediated dUDP nick-end labeling (TUNEL)-positive frontal cortical neurons was significantly decreased in EA group. The number of the PSD-95-positive cells and the miR-81 expression level in the frontal cortical in the EA group was dramatically increased in comparison with the other groups. In the PC12 cell validation experiment, IL-16 expression level was reduced under the condition of the miR-81 mimic treatment, while increased in the miR-81 inhibitor group. The PSD-95 protein level was up-regulated in the small interfering (si)RNA-IL16 group compared to the NC-IL16 groups with or without oxygen/glucose deprivation/reperfusion (OGD/R) conditions (P<0.05). However, this was abolished by miR-81 mimic. Conclusions:In VaD rats, EA may improve spatial learning and memory through miR-81/IL-16/PSD-95 pathway.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture of the Baihui and Shenting acupoints for vascular dementia in rats through the miR-81/IL-16/PSD-95 pathway

Ma¹,

Zhou²,

Yi³

et al. 2022

Ann Transl Med

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“…According to another study, pretreatment with 2/15 Hz EA before LI/R decreased microglial activation in the CA1 region [ 36 ]. Additionally, in AD and VD rats, MA and EA reduced the production of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β [ 77 , 78 ].…”

Section: Methodsmentioning

confidence: 99%

The neuroprotective and neural circuit mechanisms of acupoint stimulation for cognitive impairment

et al. 2023

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Cognitive impairment is a prevalent neurological disorder that burdens families and the healthcare system. Current conventional therapies for cognitive impairment, such as cholinesterase inhibitors and N-methyl-d-aspartate receptor antagonists, are unable to completely stop or reverse the progression of the disease. Also, these medicines may cause serious problems with the digestive system, cardiovascular system, and sleep. Clinically, stimulation of acupoints has the potential to ameliorate the common symptoms of a variety of cognitive disorders, such as memory deficit, language dysfunction, executive dysfunction, reduced ability to live independently, etc. There are common acupoint stimulation mechanisms for treating various types of cognitive impairment, but few systematic analyses of the underlying mechanisms in this domain have been performed. This study comprehensively reviewed the basic research from the last 20 years and found that acupoint stimulation can effectively improve the spatial learning and memory of animals. The common mechanism may be that acupoint stimulation protects hippocampal neurons by preventing apoptosis and scavenging toxic proteins. Additionally, acupoint stimulation has antioxidant and anti-inflammatory effects, promoting neural regeneration, regulating synaptic plasticity, and normalizing neural circuits by restoring brain functional activity and connectivity. Acupoint stimulation also inhibits the production of amyloid β-peptide and the phosphorylation of Tau protein, suggesting that it may protect neurons by promoting correct protein folding and regulating the degradation of toxic proteins via the autophagy-lysosomal pathway. However, the benefits of acupoint stimulation still need to be further explored in more high-quality studies in the future.

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“…Acupuncture therapy has a beneficial effect in mitigating cognitive impairment in AD [ 215 , 216 ]. Recent research has shown that EA treatment improves neuroinflammation and thus cognitive dysfunction in mice with AD [ 217 , 218 ]. EA therapy inhibited microglial activation, which showed that electroacupuncture at GV 20 and ST 36 points could relieve neuroinflammation effectively and thus reduce cognitive impairment.…”

Section: Application Of Therapies Targeting Tlr4 In Admentioning

confidence: 99%

Toll-Like Receptor 4: A Promising Therapeutic Target for Alzheimer’s Disease

Xia

et al. 2022

Mediators of Inflammation

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease that primarily manifests as memory deficits and cognitive impairment and has created health challenges for patients and society. In AD, amyloid β-protein (Aβ) induces Toll-like receptor 4 (TLR4) activation in microglia. Activation of TLR4 induces downstream signaling pathways and promotes the generation of proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), which also trigger the activation of astrocytes and influence amyloid-dependent neuronal death. Therefore, TLR4 may be an important molecular target for treating AD by regulating neuroinflammation. Moreover, TLR4 regulates apoptosis, autophagy, and gut microbiota and is closely related to AD. This article reviews the role of TLR4 in the pathogenesis of AD and a range of potential therapies targeting TLR4 for AD. Elucidating the regulatory mechanism of TLR4 in AD may provide valuable clues for developing new therapeutic strategies for AD.

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“Olfactory Three-Needle” Enhances Spatial Learning and Memory Ability in SAMP8 Mice

Cited by 12 publications

References 39 publications

Electroacupuncture of the Baihui and Shenting acupoints for vascular dementia in rats through the miR-81/IL-16/PSD-95 pathway

Electroacupuncture of the Baihui and Shenting acupoints for vascular dementia in rats through the miR-81/IL-16/PSD-95 pathway

The neuroprotective and neural circuit mechanisms of acupoint stimulation for cognitive impairment

Toll-Like Receptor 4: A Promising Therapeutic Target for Alzheimer’s Disease

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