Interaction of human IAPP and Aβ1-42 aggravated the AD-related pathology and impaired the cognition in mice

Chen, Haichao; Cao, Jia-Xin; Cai, Yiting; Du, Hong-Li; Xi, Xiao-Xia; Sun, Jing; Yin, Jie; Gao, Liping; Jing, Yu‐Hong

doi:10.1016/j.expneurol.2020.113490

Cited by 7 publications

(3 citation statements)

References 68 publications

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“…Chen et al (17) explored the association between A β1-42 in diabetes mellitus and Alzheimer's disease, and the results showed that the continuous increase of Aβ1-42 in the body can significantly promote the pathological changes of Alzheimer's disease in diabetic patients. Akhbari et al (18) investigated the level of free Mir-155 in patients with different degrees of diabetes.The results showed that the level of Mir-155 in serum of diabetic patients was significantly lower than that of the healthy group, and there was no significant difference in the level of Mir-155 in patients with different degrees of diabetes.…”

Section: Predictive Efficacy Of Pparγ Aβ1-42 and Mir-155 Levels On The Occurrence And Development Of Diabetes Mellitusmentioning

confidence: 99%

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Wang²,

Yu³

2022

Cell Mol Biol (Noisy-le-grand)

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The objective of this research was to study the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes. For this purpose, 52 patients with diabetes who were hospitalized from September 2019 to May 2021 were selected as the research objects. They were grouped according to the severity of the disease, which was pre-diabetes (n=16), mild (n=25), and moderate (n=16). =11), another 20 healthy subjects were taken as the control group, and the levels of PPARγ, Aβ1-42, miR-155 in each group were measured, and the correlation between changes in the levels of various indicators and the occurrence and development of diabetes was explored. Results showed that comparison of age, gender, course of disease, BMI, living habits, comorbidities, and high-density lipoprotein among the groups of diabetic patients (P>0.05); the levels of total cholesterol, triglycerides and low-density cholesterol decreased with the development of diabetes (P<0.05) ); Compared with the healthy group, the levels of PPARγ and miR-155 were significantly reduced, and the levels of Aβ1-42 were significantly increased (P<0.05); compared with the prediabetes, the levels of mild and moderate PPARγ and miR-155 showed a downward trend, and Aβ1 -42 level showed an upward trend (P<0.05); PPARγ and miR-155 levels were negatively correlated with pre-diabetes, mild, and moderate; Aβ1-42 was positively correlated with pre-diabetes, mild, and moderate (P<0.05) ; PPARγ, Aβ1-42, miR-155 levels can effectively predict the occurrence and development of diabetes, and the sensitivity, specificity and accuracy of the detection of diabetes by various indicators, positive predictive value and negative predictive value are significantly higher. It is concluded that PPARγ, Aβ1-42, miR-155 are closely related to the occurrence and development of diabetes, and there are many influencing factors of diabetes. Clinical intervention measures can be taken according to specific conditions.

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Section: Predictive Efficacy Of Pparγ Aβ1-42 and Mir-155 Levels On The Occurrence And Development Of Diabetes Mellitusmentioning

confidence: 99%

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Wang²,

Yu³

2022

Cell Mol Biol (Noisy-le-grand)

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“…Herein, we screened 12 key substances containing proteins 1–6 and 4l of NADH dehydrogenases on complex I, Cyt-C on complex III, cyt 1–3 of cytochrome oxidase on complex IV and ATP synthetases 6 and 8 (Table S1). Figure S19 found that the expression of cyt-3 and protein 6 decreased significantly after glutamate stimulation, and recovered after the addition of H 2 S. The results suggested that H 2 S can maintain the activity of cyt-3 and protein 6, which means that it can mitigate the damage of mitochondria caused by glutamate. WB (Figure C) and the quantitative results (Figure S20A) showed that the expression of cytochrome C decreased significantly after glutamate stimulation compared with the control group, but recovered significantly after the addition of NaSH.…”

Section: Resultsmentioning

confidence: 92%

Simultaneous Sensing of H₂S and ATP with a Two-Photon Fluorescent Probe in Alzheimer’s Disease: toward Understanding Why H₂S Regulates Glutamate-Induced ATP Dysregulation

Sun

Chen

et al. 2022

Anal. Chem.

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Energy deprivation and reduced levels of hydrogen sulfide (H2S) in the brain is closely associated with Alzheimer’s disease (AD). However, there is currently no fluorescent probe for precise exploration of both H2S and adenosine triphosphate (ATP) to directly demonstrate their relationship and their dynamic pattern changes. Herein, we developed a two-photon fluorescent probe, named AD-3, to simultaneously image endogenous H2S and ATP from two emission channels of fluorescent signals in live rat brains with AD. The probe achieved excellent selectivity and good detection linearity for H2S in the 0–100 μM concentration range and ATP in the 2–5 mM concentration range, respectively, with a detection limit of 0.19 μM for H2S and 0.01 mM for ATP. Fluorescence imaging in live cells reveals that such probe could successfully apply for simultaneous imaging and accurate quantification of H2S and ATP in neuronal cells. Further using real-time quantitative polymerase chain reaction and Western blots, we confirmed that H2S regulates ATP synthesis by acting on cytochrome C, cytochrome oxidase subunit 3 of complex IV, and protein 6 of complex I in the mitochondrial respiratory chain. Subsequently, we constructed a high-throughput screening platform based on AD-3 probe to rapidly screen the potential anti-AD drugs to control glutamate-stimulated oxidative stress associated with abnormal H2S and ATP levels. Significantly, AD-3 probe was found capable of imaging of H2S and ATP in APP/PS1 mice, and the concentration of H2S and ATP in the AD mouse brain was found to be lower than that in wild-type mice.

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“…The pathology of AD is characterized by progressive loss of synapses and neurons in the hippocampus and cerebral cortex [ 2 ]. The typical pathological signs of AD are senile plaques formed by the deposition of insoluble β-amyloid (Aβ) proteins outside neurons and nerve fiber tangles formed by the aggregation of highly phosphorylated Tau (p-tau) protein inside neurons [ 3 , 4 ]. There are several hypotheses on the etiology and pathogenesis of AD.…”

Section: Introductionmentioning

confidence: 99%

Expression of ITPR2 regulated by lncRNA-NONMMUT020270.2 in LPS-stimulated HT22 cells

Liu,

Tang,

Wang

et al. 2024

Heliyon

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Interaction of human IAPP and Aβ1-42 aggravated the AD-related pathology and impaired the cognition in mice

Cited by 7 publications

References 68 publications

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Simultaneous Sensing of H₂S and ATP with a Two-Photon Fluorescent Probe in Alzheimer’s Disease: toward Understanding Why H₂S Regulates Glutamate-Induced ATP Dysregulation

Expression of ITPR2 regulated by lncRNA-NONMMUT020270.2 in LPS-stimulated HT22 cells

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Interaction of human IAPP and Aβ1-42 aggravated the AD-related pathology and impaired the cognition in mice

Cited by 7 publications

References 68 publications

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Study on the correlation between PPARγ, Aβ1-42, miR-155 and the occurrence and development of diabetes

Simultaneous Sensing of H2S and ATP with a Two-Photon Fluorescent Probe in Alzheimer’s Disease: toward Understanding Why H2S Regulates Glutamate-Induced ATP Dysregulation

Expression of ITPR2 regulated by lncRNA-NONMMUT020270.2 in LPS-stimulated HT22 cells

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Simultaneous Sensing of H₂S and ATP with a Two-Photon Fluorescent Probe in Alzheimer’s Disease: toward Understanding Why H₂S Regulates Glutamate-Induced ATP Dysregulation