Marked Response of Rat Ileal and Colonic Microbiota After the Establishment of Alzheimer’s Disease Model With Bilateral Intraventricular Injection of Aβ (1-42)

Xu, Qing; Wen, Lingmiao; Wei, Guihua; Zhao, Xing‐Ming; Liu, Yanjun; Xiong, Wei; Zhang, Tinglan; Fan, Yuqing; Chen, Chunlan; Xiang, Chunxiao; Chen, Chang; Chen, Yunhui; Yin, Qian; Zhang, Tiane; Zhang, Yan

doi:10.3389/fmicb.2022.819523

Cited by 8 publications

(4 citation statements)

References 54 publications

(54 reference statements)

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“…These results suggested that Aβ 1–42 i.c.v can cause the alteration in the abundance of gut microbiota. In AD rat model caused by Aβ 1–42 i.c.v, Xu et al reported that Aβ injection could also cause the alteration in gut microflora at 4 weeks, which was consistent with our results [ 32 ]. In the analysis of gut microbiota abundance at the genus level, we found a decrease in the abundance of Alloprevotella , Ruminiclostridium , and Streptococcus , and an increase in the abundance of Akkermansia , Rikenella , and Adlercreutzia in the Aβ-treated group.…”

Section: Discussionsupporting

confidence: 93%

Injection of amyloid-β to lateral ventricle induces gut microbiota dysbiosis in association with inhibition of cholinergic anti-inflammatory pathways in Alzheimer’s disease

Qian

Liu

Chen

et al. 2022

J Neuroinflammation

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Background Alzheimer's disease (AD) is the most common neurodegenerative disease and its pathogenesis is still unclear. There is dysbiosis of gut microbiota in AD patients. More importantly, dysbiosis of the gut microbiota has been observed not only in AD patients, but also in patients with mild cognitive impairment (MCI). However, the mechanism of gut microbiota dysbiosis in AD is poorly understood. Cholinergic anti-inflammatory pathway is an important pathway for the central nervous system (CNS) regulation of peripheral immune homeostasis, especially in the gut. Therefore, we speculated that dysfunction of cholinergic anti-inflammatory pathway is a potential pathway for dysbiosis of the gut microbiota in AD. Methods In this study, we constructed AD model mice by injecting Aβ1–42 into the lateral ventricle, and detected the cognitive level of mice by the Morris water maze test. In addition, 16S rDNA high-throughput analysis was used to detect the gut microbiota abundance of each group at baseline, 2 weeks and 4 weeks after surgery. Furthermore, immunofluorescence and western blot were used to detect alteration of intestinal structure of mice, cholinergic anti-inflammatory pathway, and APP process of brain and colon in each group. Results Aβ1–42 i.c.v induced cognitive impairment and neuron damage in the brain of mice. At the same time, Aβ1–42 i.c.v induced alteration of gut microbiota at 4 weeks after surgery, while there was no difference at the baseline and 2 weeks after surgery. In addition, changes in colon structure and increased levels of pro-inflammatory factors were detected in Aβ1–42 treatment group, accompanied by inhibition of cholinergic anti-inflammatory pathways. Amyloidogenic pathways in both the brain and colon were accelerated in Aβ1–42 treatment group. Conclusions The present findings suggested that Aβ in the CNS can induce gut microbiota dysbiosis, alter intestinal structure and accelerate the amyloidogenic pathways, which were related to inhibiting cholinergic anti-inflammatory pathways.

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Section: Discussionsupporting

confidence: 93%

Injection of amyloid-β to lateral ventricle induces gut microbiota dysbiosis in association with inhibition of cholinergic anti-inflammatory pathways in Alzheimer’s disease

Qian

Liu

Chen

et al. 2022

J Neuroinflammation

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“…Each 25 μL reaction comprised 1X PCR buffer, 1.5 mM MgCl2, 0.4 μM dNTPs, 1.0 μM each of forward and reverse primers, 0.5 U TOYOBO KOD-Plus-Neo enzyme (Toyobo; Osaka, Japan; KOD-401B), and 10 ng of the template. The PCR program was set as follows: initial denaturation at 94 °C for 1 min; 30 cycles of denaturation at 94 °C for 20 s, annealing at 54 °C for 30 s, and extension at 72 °C for 30 s; and a final elongation step at 72 °C for 5 min [ 44 ].…”

Section: Methodsmentioning

confidence: 99%

Differential Response of Ileal and Colonic Microbiota in Rats with High-Fat Diet-Induced Atherosclerosis

Wen

Xiong

Wei

et al. 2022

IJMS

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Growing evidence suggests that gut microbiota are associated with atherosclerosis (AS). However, the functional heterogeneity of each gut segment gives rise to regional differences in gut microbiota. We established a rat model of AS by feeding the rats a high-fat diet for a long period. The pathological and microbiota changes in the ileum and colon of the rats were examined, and correlations between AS and microbiota were analyzed. The aortic mesothelium of the experimental rats was damaged. The intima showed evident calcium salt deposition, indicating that the AS rat model was successfully developed. We noted varying degrees of pathological damage in the ileum and colon of the experimental rats. The 16S rDNA high-throughput sequencing showed significant differences in α-diversity, β-diversity, and microbiota comparisons in the ileum and colon. Furthermore, the ileum and colon of AS rats showed varying degrees of intestinal microbiota disturbance. This article contributes to the study of the relationship between the microbiota in different regions of the gut and AS, and provides new approaches in gut microbiota intervention for the treatment of AS.

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“…According to previous reports, Cef (200 mg/kg) and DHK (10 mg/kg) were administered to the corresponding groups by intraperitoneal injection once a day for 7 consecutive days [29,31]. Aβ was administered once in corresponding groups by right lateral ventricle injection (5 μl, 2 μg/μl, 10 μg in total) [32,33]. USP46 siRNA (2 μl, 0.5 μg/μl, 1 μg in total) was administered once to the corresponding groups by microinjection into the CA1 region of the right hippocampus [34].…”

Section: Animals and Groupingmentioning

confidence: 99%

“…The solution was oscillated vigorously using an oscillator until dissolution. The dissolved Aβ solution was incubated at 37 ℃ for 7 days for oligomerization [32][33]. USP46 siRNA and negative control sequences were designed and synthesized by Shanghai Sangong Bioengineering Company (Shanghai, China).…”

Section: Antibodies and Reagentsmentioning

confidence: 99%

Ceftriaxone Modulates Ubiquitination of α-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid Receptors to Improve Long-Term Potentiation Impairment Induced by Exogenous β-Amyloid in a Glutamate Transporter-1 Dependent Manner

Jiang,

Li,

Wang

et al. 2024

Mol Neurobiol

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α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) are crucial for properties of synaptic plasticity, such as long-term potentiation (LTP). LTP impairment can occur early in the onset of Alzheimer's disease (AD). The downregulation or decreased abundance of AMPAR expression in the postsynaptic membrane is closely associated with LTP impairment. Ceftriaxone (Cef) can improve LTP impairment in the early stages of AD in a mouse model. The purpose of this study was to explore the mechanism underlying this process from the aspects of AMPAR expression and ubiquitination degree. In this study, we found that β-amyloid (Aβ) treatment induced hippocampal LTP impairment and AMPAR downregulation and ubiquitination. Cef pretreatment ameliorated Aβ-induced hippocampal LTP impairment, reduced AMPAR ubiquitination, and increased AMPAR expression, especially in the plasma membrane, in Aβ-treated mice. Administration of USP46 siRNA and DHK (a speci c blocker of glutamate transporter-1) signi cantly inhibited the above effects of Cef, suggesting a role for anti-AMPAR ubiquitination and upregulation of glutamate transporter-1 (GLT-1) in the Cef-induced improvements mentioned above. The above ndings demonstrate that pretreatment with Cef effectively mitigated Aβinduced impairment of hippocampal LTP by suppressing the ubiquitination process of AMPARs in a GLT-1-dependent manner. These results provide novel insights into the underlying mechanisms elucidating the anti-AD by Cef.

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Marked Response of Rat Ileal and Colonic Microbiota After the Establishment of Alzheimer’s Disease Model With Bilateral Intraventricular Injection of Aβ (1-42)

Cited by 8 publications

References 54 publications

Injection of amyloid-β to lateral ventricle induces gut microbiota dysbiosis in association with inhibition of cholinergic anti-inflammatory pathways in Alzheimer’s disease

Injection of amyloid-β to lateral ventricle induces gut microbiota dysbiosis in association with inhibition of cholinergic anti-inflammatory pathways in Alzheimer’s disease

Differential Response of Ileal and Colonic Microbiota in Rats with High-Fat Diet-Induced Atherosclerosis

Ceftriaxone Modulates Ubiquitination of α-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid Receptors to Improve Long-Term Potentiation Impairment Induced by Exogenous β-Amyloid in a Glutamate Transporter-1 Dependent Manner

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