scholarly journals Exendin-4 antagonizes Aβ1-42-induced attenuation of spatial learning and memory ability

2016 ◽  
Vol 12 (5) ◽  
pp. 2885-2892 ◽  
Author(s):  
Xiaohui Wang ◽  
Li Wang ◽  
Ruirui Jiang ◽  
Yunyun Xu ◽  
Xueling Zhao ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
Memory Ability

scholarly journals Caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1 in Alzheimer’s disease

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Xunhu Gu ◽  
Hanjun Wu ◽  
Yuqin Xie ◽  
Lijun Xu ◽  
Xu Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Membrane Transport ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Senile Plaque ◽  
Spatial Learning And Memory ◽  
Memory Ability ◽  
Caspase 1 ◽  
Plaque Deposition

Abstract Background Alzheimer's disease is a neurodegenerative disease. Previous study has reported that caspase-1/IL-1β is closely associated with Alzheimer's disease. However, the biological role of caspase-1/IL-1β in Alzheimer's disease has not been fully elucidated. This study aimed to explore the mechanism of action of caspase-1/IL-1β in Alzheimer's disease. Methods Mouse hippocampal neurones were treated with Aβ1-42 to induce Alzheimer's disease cell model. APP/PS1 mice and Aβ1-42-induced hippocampal neurones were treated with AC-YVAD-CMK (caspase-1 inhibitor). Spatial learning and memory ability of mice were detected by morris water maze. Flow cytometry, TUNEL staining, Thioflavin S staining and immunohistochemistry were performed to examine apoptosis and senile plaque deposition. Enzyme linked immunosorbent assay and western blot were performed to assess the levels of protein or cytokines. Co-Immunoprecipitation was performed to verify the interaction between Stargazin and GluA1. Results AC-YVAD-CMK treatment improved spatial learning and memory ability and reduced senile plaque deposition of APP/PS1 mice. Moreover, AC-YVAD-CMK promoted membrane transport of GluA1 in APP/PS1 mice. In vitro, Aβ1-42-induced hippocampal neurones exhibited an increase in apoptosis and a decrease in the membrane transport of GluA1, which was abolished by AC-YVAD-CMK treatment. In addition, Stargazin interacted with GluA1, which was repressed by caspase-1. Caspase-1/IL-1β inhibited membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1. Conclusions Our data demonstrate that caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin in Alzheimer's disease. Thus, caspase-1/IL-1β may be a target for Alzheimer's disease treatment.

scholarly journals Taurine improves the spatial learning and memory ability impaired by sub-chronic manganese exposure

2014 ◽  
Vol 21 (1) ◽  
pp. 51 ◽  
Author(s):  
Cai-Ling Lu ◽  
Shen Tang ◽  
Zhi-Juan Meng ◽  
Yi-Yuan He ◽  
Ling-Yong Song ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
Memory Ability ◽  
Manganese Exposure

scholarly journals Deficiency of Intellectual Disability-Related Gene Brpf1 Attenuated Hippocampal Excitatory Synaptic Transmission and Impaired Spatial Learning and Memory Ability

2021 ◽  
Vol 9 ◽  
Author(s):  
Weiwei Xian ◽  
Jingli Cao ◽  
Xiangshan Yuan ◽  
Guoxiang Wang ◽  
Qiuyan Jin ◽  
...  
Keyword(s):  
Intellectual Disability ◽  
Synaptic Transmission ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Hippocampal Neurons ◽  
Dendritic Morphology ◽  
Excitatory Synaptic Transmission ◽  
Spatial Learning And Memory ◽  
Memory Ability ◽  
Cultured Hippocampal Neurons

Patients with monoallelic bromodomain and PHD finger-containing protein 1 (BRPF1) mutations showed intellectual disability. The hippocampus has essential roles in learning and memory. Our previous work indicated that Brpf1 was specifically and strongly expressed in the hippocampus from the perinatal period to adulthood. We hypothesized that mouse Brpf1 plays critical roles in the morphology and function of hippocampal neurons, and its deficiency leads to learning and memory deficits. To test this, we performed immunofluorescence, whole-cell patch clamp, and mRNA-Seq on shBrpf1-infected primary cultured hippocampal neurons to study the effect of Brpf1 knockdown on neuronal morphology, electrophysiological characteristics, and gene regulation. In addition, we performed stereotactic injection into adult mouse hippocampus to knock down Brpf1 in vivo and examined the learning and memory ability by Morris water maze. We found that mild knockdown of Brpf1 reduced mEPSC frequency of cultured hippocampal neurons, before any significant changes of dendritic morphology showed. We also found that Brpf1 mild knockdown in the hippocampus showed a decreasing trend on the spatial learning and memory ability of mice. Finally, mRNA-Seq analyses showed that genes related to learning, memory, and synaptic transmission (such as C1ql1, Gpr17, Htr1d, Glra1, Cxcl10, and Grin2a) were dysregulated upon Brpf1 knockdown. Our results showed that Brpf1 mild knockdown attenuated hippocampal excitatory synaptic transmission and reduced spatial learning and memory ability, which helps explain the symptoms of patients with BRPF1 mutations.

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

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yuan Wang ◽  
Qiang Wang ◽  
Bo Ren ◽  
Ting Guo ◽  
Jing Qiang ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Olfactory System ◽  
Spatial Learning And Memory ◽  
Neuroinflammatory Response ◽  
Memory Ability ◽  
Amyloid A ◽  
Samp8 Mice ◽  
Excessive Activation ◽  
Stimulation Of

As one of the most important therapies in complementary and alternative medicine, acupuncture has been used in the treatment of Alzheimer’s disease (AD). Acupuncture of “olfactory three-needle” manipulation can improve the cognitive ability of AD patients. However, the mechanism of “olfactory three-needle” in AD remains largely unknown. Here, we identified that the “olfactory three-needle” therapy and eugenol olfactory stimulation both reduced the deposition of β-amyloid (Aβ) protein and increased the expression of synaptophysin (SYP), but only the “olfactory three-needle” enhanced the spatial learning and memory ability of SAMP8. Remarkably, the “olfactory three-needle” inhibited the phosphorylation of p38MAPK and the excessive activation of microglia (MG) in the hippocampus. Our study demonstrates that the “olfactory three-needle” enhances spatial learning and memory ability by inhibiting the phosphorylation of p38MAPK and the excessive activation of MG to reduce the neuroinflammatory response and neurotoxicity of Aβ and promote synaptic regeneration, but it was not completely consistent with the stimulation of the olfactory system.

Sign in / Sign up

Export Citation Format

Share Document