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174 results on '"Liang, Zhihou"'

3. Brain Gene Expression of a Sporadic (icv-STZ Mouse) and a Familial Mouse Model (3xTg-AD Mouse) of Alzheimer�s Disease

Author

Chen, Yanxing, Tian, Zhu, Liang, Zhihou, Sun, Shenggang, Dai, Chun-ling, Lee, Moon H, LaFerla, Frank M, Grundke-Iqbal, Inge, Iqbal, Khalid, Liu, Fei, Gong, Cheng-Xin, and Planel, Emmanuel

Subjects
insulin signaling pathway, triple-transgenic model, a-beta, glucose-metabolism, cognitive impairment, o-glcnacylation, nervous-system, tau, dysfunction, presenilins
Published
2012

19. 18F-APN-1607 Tau Positron Emission Tomography Imaging for Evaluating Disease Progression in Alzheimer's Disease.

Author

Xu, Xiaojun, Ruan, Weiwei, Liu, Fang, Gai, Yongkang, Liu, Qingyao, Su, Ying, Liang, Zhihou, Sun, Xun, and Lan, Xiaoli

Subjects
POSITRON emission tomography, ALZHEIMER'S disease, CEREBELLAR cortex, PARIETAL lobe, MOTOR cortex, DISEASE progression, KRUSKAL-Wallis Test, STATISTICS, ACADEMIC medical centers, TAU proteins, ONE-way analysis of variance, RETROSPECTIVE studies, SEVERITY of illness index, PEARSON correlation (Statistics), NEUROPSYCHOLOGICAL tests, RESEARCH funding, DATA analysis, SPACE perception
Abstract

Purpose: 18F-APN-1607 is a novel tau positron emission tomography (PET) tracer characterized with high binding affinity for 3− and 4-repeat tau deposits. The aim was to analyze the spatial distribution of 18F-APN-1607 PET imaging in Alzheimer's disease (AD) subjects with different stages and to investigate the relationship between the change of tau deposition and overall disease progression. Methods: We retrospectively analyzed the 18F-APN-1607 PET imaging of 31 subjects with clinically and imaging defined as AD. According to the Mini-Mental State Examination (MMSE) score, patients were divided into three groups, namely, mild (≥21, n = 7), moderate (10–20, n = 16), and severe (≤9, n = 8). PET imaging was segmented to 70 regions of interest (ROIs) and extracted the standard uptake value (SUV) of each ROI. SUV ratio (SUVR) was calculated from the ratio of SUV in different brain regions to the cerebellar cortex. The regions were defined as positive and negative with unsupervised cluster analysis according to SUVR. The SUVRs of each region were compared among groups with the one-way ANOVA or Kruskal–Wallis H test. Furthermore, the correlations between MMSE score and regional SUVR were calculated with Pearson or Spearman correlation analysis. Results: There were no significant differences among groups in gender (χ2 = 3.814, P = 0.161), age of onset (P = 0.170), age (P = 0.109), and education level (P = 0.065). With the disease progression, the 18F-APN-1607 PET imaging showed the spread of tau deposition from the hippocampus, posterior cingulate gyrus (PCG), and lateral temporal cortex (LTC) to the parietal and occipital lobes, and finally to the frontal lobe. Between the mild and moderate groups, the main brain areas with significant differences in 18F-APN-1607 uptake were supplementary motor area (SMA), cuneus, precuneus, occipital lobule, paracentral lobule, right angular gyrus, and parietal, which could be used for early disease progression assessment (P < 0.05). There were significant differences in the frontal lobe, right temporal lobe, and fusiform gyrus between the moderate and severe groups, which might be suitable for the late-stage disease progression assessment (P < 0.05). Conclusion: 18F-APN-1607 PET may serve as an effective imaging marker for visualizing the change pattern of tau protein deposition in AD patients, and its uptake level in certain brain regions is closely related to the severity of cognitive impairment. These indicate the potential of 18F-APN-1607 PET for the in vivo evaluation of the progression of AD. [ABSTRACT FROM AUTHOR]

Published
2022
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21. Sixteen-Week Interventional Study to Evaluate the Clinical Effects and Safety of Rivastigmine Capsules in Chinese Patients with Alzheimer’s Disease

Author

Jia, Jianping, primary, Ji, Yong, additional, Feng, Tao, additional, Ye, Qinyong, additional, Peng, Dantao, additional, Kuang, Weihong, additional, Ning, Yuping, additional, Liang, Zhihou, additional, Fan, Dongsheng, additional, Wei, Wenshi, additional, Li, Yansheng, additional, and Xiao, Shifu, additional

Published
2019
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26. Chinese Language Screening Test

Author

Yang, Hongyan, primary, Tian, Shenghua, additional, Flamand-Roze, Constance, additional, Gao, Ling, additional, Zhang, Wei, additional, Li, Yan, additional, Wang, Jiajia, additional, Sun, Zhou, additional, Su, Ying, additional, Zhao, Libin, additional, and Liang, Zhihou, additional

Published
2018
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28. Intracerebroventricular streptozotocin exacerbates Alzheimer-like changes of 3xTg-AD mice1

Author

Chen, Yanxing, Liang, Zhihou, Tian, Zhu, Blanchard, Julie, Dai, Chun-ling, Chalbot, Sonia, Iqbal, Khalid, Liu, Fei, and Gong, Cheng-Xin

Subjects
Mice, Inbred C57BL, Disease Models, Animal, Mice, Mice, 129 Strain, Alzheimer Disease, Animals, Brain, Female, Mice, Transgenic, Maze Learning, Article, Streptozocin, Injections, Intraventricular
Abstract

Alzheimer's disease (AD) involves several possible molecular mechanisms, including impaired brain insulin signaling and glucose metabolism. To investigate the role of metabolic insults in AD, we injected streptozotocin (STZ), a diabetogenic compound if used in the periphery, into the lateral ventricle of the 6-month-old 3xTg-AD mice and studied the cognitive function as well as AD-like brain abnormalities, such as tau phosphorylation and Aβ accumulation, 3-6 weeks later. We found that STZ exacerbated impairment of short-term and spatial reference memory in 3xTg-AD mice. We also observed an increase in tau hyperphosphorylation and neuroinflammation, a disturbance of brain insulin signaling, and a decrease in synaptic plasticity and amyloid β peptides in the brain after STZ treatment. The expression of 20 AD-related genes, including those involved in the processing of amyloid precursor protein, cytoskeleton, glucose metabolism, insulin signaling, synaptic function, protein kinases, and apoptosis, was altered, suggesting that STZ disturbs multiple metabolic and cell signaling pathways in the brain. These findings provide experimental evidence of the role of metabolic insult in AD.

Published
2013

29. Intranasal Insulin Prevents Anesthesia-induced Cognitive Impairments in Aged Mice

Author

Li, Xing, Run, Xiaoqin, Wei, Zhen, Zeng, Kuan, Liang, Zhihou, Huang, Fang, Ke, Dan, Wang, Qun, Wang, Jian-Zhi, Liu, Rong, Zhang, Bin, and Wang, Xiaochuan

Abstract

Background: Preclinical and clinical evidence suggests that elderly individuals are at increased risk of cognitive decline after general anesthesia. General anesthesia is also believed to be a risk factor for Postoperative Cognitive Dysfunction (POCD) and Alzheimer's Disease (AD). Intranasal administration of insulin, which delivers the drug directly into the brain, improves memory and cognition in both animal studies and small clinical trials. However, how insulin treatment improves cognitive function is poorly understood. Methods: Aged mice were pretreated with intranasal insulin or saline before anesthesia. Propofol was added intraperitoneally to the mice from 7th day of insulin/saline treatment, and general anesthesia was induced and maintained for 2 hours/day for 5 consecutive days. Mice were evaluated at 26th day when the mice were continued on insulin or saline administration for another 15 days. Results: We found that intranasal insulin treatment prevented anesthesia-induced cognitive impairments, as measured by novel object recognition test and contextual-dependent fear conditioning test. Insulin treatment also increased the expression level of Post-synaptic Density Protein 95 (PSD95), as well as upregulated Microtubule-associated Protein-2 (MAP-2) in the dentate gyrus of the hippocampus. Furthermore, we found that insulin treatment restored insulin signaling disturbed by anesthesia via activating PI3K/PDK1/AKT pathway, and attenuated anesthesia-induced hyperphosphorylation of tau at multiple AD-associated sites. We found the attenuation of tau hyperphosphorylation occurred by increasing the level of GSK3β phosphorylated at Ser9, which leads to inactivation of GSK-3β. Conclusion: Intranasal insulin administration might be a promising therapy to prevent anesthesiainduced cognitive deficit in elderly individuals.

Published
2019
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31. Differential Effects of an O-GlcNAcase Inhibitor on Tau Phosphorylation

Author

Yu, Yang, Zhang, Lan, Li, Xiaojing, Run, Xiaoqin, Liang, Zhihou, Li, Yi, Liu, Ying, Lee, Moon, Grundke-Iqbal, Inge, Iqbal, Kalid, and Vocadlo, David

Abstract

Abnormal hyperphosphorylation of microtubule-associated protein tau plays a crucial role in neurodegeneration in Alzheimer's disease (AD). The aggregation of hyperphosphorylated tau into neurofibrillary tangles is also a hallmark brain lesion of AD. Tau phosphorylation is regulated by tau kinases, tau phosphatases, and O-GlcNAcylation, a posttranslational modification of proteins on the serine or threonine residues with β-N-acetylglucosamine (GlcNAc). O-GlcNAcylation is dynamically regulated by O-GlcNAc transferase, the enzyme catalyzing the transfer of GlcNAc to proteins, and N-acetylglucosaminidase (OGA), the enzyme catalyzing the removal of GlcNAc from proteins. Thiamet-G is a recently synthesized potent OGA inhibitor, and initial studies suggest it can influence O-GlcNAc levels in the brain, allowing OGA inhibition to be a potential route to altering disease progression in AD. In this study, we injected thiamet-G into the lateral ventricle of mice to increase O-GlcNAcylation of proteins and investigated the resulting effects on site-specific tau phosphorylation. We found that acute thiamet-G treatment led to a decrease in tau phosphorylation at Thr181, Thr212, Ser214, Ser262/Ser356, Ser404 and Ser409, and an increase in tau phosphorylation at Ser199, Ser202, Ser396 and Ser422 in the mouse brain. Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3β (GSK-3β), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT. However, the elevation of tau phosphorylation at the sites above was not observed and GSK-3β was not activated in cultured adult hippocampal progenitor cells or in PC12 cells after thiamet-G treatment. These results suggest that acute high-dose thiamet-G injection can not only directly antagonize tau phosphorylation, but also stimulate GSK-3β activity, with the downstream consequence being site-specific, bi-directional regulation of tau phosphorylation in the mammalian brain.

Published
2012

41. Differential Effects of an O-GlcNAcase Inhibitor on Tau Phosphorylation

Author

Yu, Yang, primary, Zhang, Lan, additional, Li, Xiaojing, additional, Run, Xiaoqin, additional, Liang, Zhihou, additional, Li, Yi, additional, Liu, Ying, additional, Lee, Moon H., additional, Grundke-Iqbal, Inge, additional, Iqbal, Khalid, additional, Vocadlo, David J., additional, Liu, Fei, additional, and Gong, Cheng-Xin, additional

Published
2012
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48. Stereotaxical Infusion of Rotenone: A Reliable Rodent Model for Parkinson's Disease

Author

Xiong, Nian, primary, Huang, Jinsha, additional, Zhang, Zhentao, additional, Zhang, Zhaowen, additional, Xiong, Jing, additional, Liu, Xingyuan, additional, Jia, Min, additional, Wang, Fang, additional, Chen, Chunnuan, additional, Cao, Xuebing, additional, Liang, Zhihou, additional, Sun, Shenggang, additional, Lin, Zhicheng, additional, and Wang, Tao, additional

Published
2009
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