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Authors: Li, Fangyu | Qin, Wei | Zhu, Min | Jia, Jianping

Article Type: Research Article

Abstract: Background: Current and future incidence and prevalence estimates of dementia are essential for public health planning. Objective: The objective was to establish prediction model of incidence and estimate the prevalence of dementia in the Chinese and worldwide population from 2020 to 2050. Methods: A model-based method was used to project the dementia prevalence from 2020 to 2050 in China, which required incidence, the mortality rate for individual without dementia, and the relative risk of death. Furthermore, we detected the impact of intervention on the prevalence projection for dementia using a simulation method. We applied the same method to other projections …worldwide. Results: In 2020, the model predicted 16.25 million (95%confidence interval 11.55–21.18) persons with dementia in China. By 2050, this number would increase by approximately three-fold to 48.98 million (38.02–61.73). Through data simulation, if the incidence of dementia decreased by 10%every 10 years from 2020 after intervention and prevention, the number of dementia cases by 2050 was reduced by 11.96 million. This would reduce the economic burden by US $639.04 billion. In addition, using this model, dementia cases grew relatively slowly over the next few decades in the United States of America, the United Kingdom, and Japan, with percentage changes of 100.88%, 65.93%, and 16.20%, respectively. Conclusion: The number of people with dementia in China is large and will continue to increase rapidly. Effective interventions could reduce the number of patients drastically. Therefore, prevention and control strategies must be formulated urgently to reduce the occurrence of dementia. Show more

Keywords: China, dementia, model-based, prevalence, projection

DOI: 10.3233/JAD-210493

Citation: Journal of Alzheimer's Disease, vol. 82, no. 4, pp. 1823-1831, 2021

Authors: Su, Jing | Zhu, Wenting | Liu, Jing | Yin, Jian | Qin, Wei | Jiang, Changbin

Article Type: Research Article

Abstract: The aim of the present study was to research the role of nitric oxide (NO) as a mediator of alpha (α)-asarone effect at the pentylenetetrazol (PTZ)-induced epileptiform discharge in rat. α-Asarone that was injected intraperitoneally twenty minutes before PTZ injection suppressed the clonic discharge effectively and the significant actions lasted for 30 min with no change of clonic amplitude. Administration of α-asarone did not influence interictal discharge. Four kinds of NO regulators were administered, including non-selective NG-nitro-L-arginine methyl ester (L-NAME), selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG) and NO substrate, …L-arginine (ARG) and their influence on the actions of α-asarone were studied, and all of the regulators were administered fifteen minutes before α-asarone injection. L-NAME and 7-NI reversed the anticlonic activity of α-asarone, and a significant increase of clonic activity was induced by L-NAME later in L-NAME + .α-asarone + PTZ group. There were no significant differences between AG + α-asarone + PTZ and α-asarone + PTZ group. L-ARG played a dual role in this study. It aggravated clonic discharge in the early stage but relieved interictal discharge in the late stage compared with PTZ group alone, and the beneficial effect of α-asarone was also reversed. All the above results suggest that nNOS/NO pathway mediates the anticonvulsant effect of α-asarone, and NO played a biphasic role in PTZ modeling process, while iNOS was unrelated to the inhibition effect of α-asarone on PTZ induced epileptiform activity. Show more

Keywords: Alpha-asarone, epileptiform activity, nitric oxide synthase, pentylenetetrazol

DOI: 10.3233/BME-141192

Citation: Bio-Medical Materials and Engineering, vol. 24, no. 6, pp. 3645-3655, 2014

Authors: Li, Xuanting | Yuan, Junliang | Qin, Wei | Yang, Lei | Yang, Shuna | Li, Yue | Hu, Wenli

Article Type: Research Article

Abstract: Background: Cerebral microbleed (CMB) is an increasingly important risk factor for cognitive impairment due to population aging. Controversies, however, remain regarding the exact association between CMB and cognitive dysfunction. Objective: We aimed to determine the relationship between CMB burden and cognitive impairment, and also explore the characteristics of cognitive decline in CMB patients for middle-aged and elderly people. Methods: The present cross-sectional study included 174 participants (87 CMB patients and 87 controls) who underwent brain magnetic resonance imaging and a battery of neuropsychological test. Global cognitive function was measured using Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Compound …z-scores were calculated for three cognitive subdomains: memory, executive function and processing speed. Results: CMB patients had lower scores of MMSE (p  < 0.001) and MoCA (p  < 0.001). Patients at each category of CMB count had worse performance in global cognitive function and all three cognitive subdomains (p  < 0.001). In multiple linear regression models, CMB patients had significantly greater declines in executive function (p  < 0.001), processing speed (p  < 0.001), and MoCA (p  = 0.003) with increasing number of CMB. We found no relationship between CMB location and cognition (p  > 0.05). Conclusion: CMB is associated with impairment in global cognition as well as for all tested subdomains. Strongest effect sizes were seen for tests which rely on executive functioning, where performance deficits increased in proportion to degree of CMB burden. Prospective studies are needed to evaluate whether the association between CMB and executive dysfunction is causal. Show more

Keywords: Cerebral microbleed, cerebral small vessel disease, cognitive impairment, susceptibility weighted imaging

DOI: 10.3233/JAD-201202

Citation: Journal of Alzheimer's Disease, vol. 81, no. 1, pp. 255-262, 2021

Authors: Xing, Yi | Tang, Yi | Zhao, Lina | Wang, Qi | Qin, Wei | Zhang, Jin-Lan | Jia, Jianping

Article Type: Research Article

Abstract: Background: Various evidence demonstrates the influences of ceramides on Alzheimer’s disease (AD) pathogenesis. Furthermore, increased ceramides were also suggested to be related to cognitive decline. However, the association between ceramides and neuropsychiatric symptoms of AD remains unclear. Objective: This study sought to investigate the association between plasma ceramide levels and multiple neuropsychiatric symptoms in AD. Methods: A total of 98 patients and 92 cognitively normal controls participated in this study, including 56 with mild AD and 42 with moderate to severe AD. The Neuropsychiatric Inventory (NPI) was used to assess neuropsychiatric symptoms. Considering the influences of dementia severity on ceramide …levels and neuropsychiatric symptoms, a subgroup analysis was conducted by dementia severity. Results: Except for C24 : 0, all ceramide species were significantly higher in AD patients than in controls. After controlling for confounding factors, the C16 : 0 and C20 : 0 levels were positively associated with delusions, and the quartiles of C22 : 0 and C24 : 0 were positively associated with depression. In the subgroup analysis, association between ceramide species and delusions were only observed in mild AD, and the association between ceramides and depression were prominent in moderate to severe AD. In mild AD, after controlling for age, gender, anti-dementia medications, diabetes status, and ApoE ɛ 4 status, the C16 : 0, C20 : 0, and quartiles of C24 : 1 were associated with delusions. In moderate to severe AD, depression was associated with C22 : 0 and C24 : 0. Conclusion: There were stage-specific associations between ceramides and neuropsychiatric symptoms of AD. The potential mechanisms deserve further investigation. Show more

Keywords: Alzheimer’s disease, ceramides, plasma, psychiatry

DOI: 10.3233/JAD-151158

Citation: Journal of Alzheimer's Disease, vol. 52, no. 3, pp. 1029-1035, 2016

Authors: Wang, Qianqian | Jia, Jianping | Qin, Wei | Wu, Liyong | Li, Dan | Wang, Qi | Li, Hanzhi

Article Type: Research Article

Abstract: Background: Mutations within exons 16 and 17 of the amyloid-β protein precursor (AβPP) gene were the first known causes of early-onset familial Alzheimer’s disease (EOFAD). Since the first AβPP mutation was reported, 39 different AβPP variations have been discovered in EOFAD. Objective: We described a novel AβPP M722K mutation found in a Chinese familial Alzheimer’s disease pedigree and confirmed its effects on amyloid-β (Aβ) secretion and tau phosphorylation. Methods: We performed direct sequencing of exons 16 and 17 of the AβPP gene and coding exons 3–12 of the PSEN1 and PSEN2 genes for genetic analysis. N2a cells were transfected with …wild-type AβPP, AβPP constructs harboring the M722K mutation, or AβPP constructs harboring the Swedish mutation to demonstrate the effects of the AβPP M722K mutation on Aβ secretion and tau phosphorylation. Results: Different phenotypes of patients carrying the AβPP M722K mutation maybe were related to different apolipoprotein E genotypes. The expression of AβPP M722K in mouse neuroblastoma N2a cells induced a 1.7-fold increased ratio of Aβ 42 to Aβ 40 without changes in sAβPPα and sAβPPβ. Tau phosphorylation at the AT8 sites was also increased. Conclusion: Maybe the AβPP M722K mutation contributed to the cause of EOFAD in this Chinese pedigree mediated by increased Aβ 42 /Aβ 40 . Further studies should be conducted to validate the pathogenicity of AβPP M722K and the interactions among γ -secretase, APOE, and AβPP. Show more

Keywords: Aβ42/Aβ40, AβPP M722K mutation, amyloid-β protein precursor, familial Alzheimer’s disease, tau phosphorylation

DOI: 10.3233/JAD-143231

Citation: Journal of Alzheimer's Disease, vol. 47, no. 1, pp. 157-165, 2015

Authors: Dong, Jing | Qin, Wei | Wei, Cuibai | Tang, Yi | Wang, Qi | Jia, Jianping

Article Type: Research Article

Abstract: Background: Presenilin-1 (PSEN1 ) is the most frequently mutated gene in familial Alzheimer’s disease (AD), whereas only several novel mutations have been reported in China and functional studies were seldom conducted. Objective: We describe a novel PSEN1 K311R mutation in two Chinese families with late-onset AD and its functional impact on amyloid-β protein precursor (AβPP) processing and tau phosphorylation. Methods: The mutation was detected by direct sequencing of PSEN1 exon 9. HEK293 cells stably expressing wild-type APP 695 (HEK293-APP 695wt ) were transfected with plasmids containing human wild-type PSEN1 , PSEN1 K311R mutation, and PSEN1 E280A mutation to compare the K311R …mutation’s effects on AβPP processing with other groups. In addition, each group of cells were co-transfected with plasmids harboring PSEN1 and human wild-type MAPT complementary DNA to study the mutation’s impacts on tau phosphorylation. Results: The K311R mutation was detected in probands of two late-onset AD families. Expression of the K311R or E280A mutation increased amyloid-β (Aβ)42 levels but decreased Aβ40 levels, resulting in an overall increase in the Aβ42 /Aβ40 ratio compared to those in wild-type PSEN1 transfected cells (p  < 0.05). The K311R or E280A mutation also increased the levels of phosphorylated tau compared to wild-type PSEN1 (p  < 0.05). Conclusion: The K311R mutation might contribute to AD pathogenesis by overproducing toxic Aβ species and enhancing tau phosphorylation. Further in-depth studies are needed to decipher the pathogenic mechanisms of the K311R mutation in terms of AβPP cleavage, tau phosphorylation, and other presenilin-1 mediated functional pathways. Show more

Keywords: Amyloid-β, familial Alzheimer’s disease, mutation, presenilin, tau

DOI: 10.3233/JAD-161188

Citation: Journal of Alzheimer's Disease, vol. 57, no. 2, pp. 613-623, 2017

Authors: Yang, Heyun | Wang, Wei | Jia, Longfei | Qin, Wei | Hou, Tingting | Wu, Qiaoqi | Li, Haitao | Tian, Yuanruhua | Jia, Jianping

Article Type: Research Article

Abstract: The blood-brain barrier (BBB) can restrict the therapeutic effects of Alzheimer’s disease (AD) medications. While a large number of AD drug treatment trials targeting BBB dynamics have emerged, most have failed due to insufficient permeability. Furthermore, a subset of AD cases, which also feature chronic hypoperfusion are complicated by BBB deficits. We used a mouse model of AD with chronic hypoperfusion—transgenic mice (PS1V97L) with right common carotid artery ligation. In this model, we assessed how chronic cerebral hypoperfusion changed the pathophysiological processes that increase BBB permeability. Compared with control mice, AD mice with chronic hypoperfusion revealed significantly upregulated expression of …the receptor for advanced glycation end products (RAGE) on the BBB. Upregulated RAGE caused increased accumulation of amyloid-β (Aβ) in the brain in these mice. Upregulation of RAGE (or binding to Aβ) can promote activation of the NF-κ B pathway and enhance oxidative stress and increase the release of pro-inflammatory factors. These factors promoted the reduction of tight junction proteins between the endothelial cells in the BBB and increased its permeability. These findings suggest that the transporter RAGE dysregulation on the BBB initiates a series of pathophysiological processes which lead to increased BBB permeability. Taken together, we have shown that chronic hypoperfusion can serve to enhance and aggravate the BBB impairment in AD. Show more

Keywords: Alzheimer’s disease, blood-brain barrier, chronic cerebral hypoperfusion, NF-κB pathway, permeability, transgenic mice

DOI: 10.3233/JAD-191045

Citation: Journal of Alzheimer's Disease, vol. 74, no. 1, pp. 261-275, 2020

Authors: Yang, Heyun | Wang, Wei | Jia, Longfei | Qin, Wei | Hou, Tingting | Wu, Qiaoqi | Li, Haitao | Tian, Yuanruhua | Jia, Jianping

Article Type: Correction

DOI: 10.3233/JAD-239007

Citation: Journal of Alzheimer's Disease, vol. 94, no. 4, pp. 1619-1622, 2023

Authors: Qin, Wei | Li, Wenwen | Wang, Qi | Gong, Min | Li, Tingting | Shi, Yuqing | Song, Yang | Li, Ying | Li, Fangyu | Jia, Jianping

Article Type: Research Article

Abstract: Background: The global race-dependent association of Alzheimer’s disease (AD) and apolipoprotein E (APOE ) genotype is not well understood. Transethnic analysis of APOE could clarify the role of genetics in AD risk across populations. Objective: This study aims to determine how race and APOE genotype affect the risks for AD. Methods: We performed a systematic search of PubMed, Embase, Web of Science, and the Cochrane Library since 1993 to Aug 25, 2020. A total of 10,395 reports were identified, and 133 were eligible for analysis with data on 77,402 participants. Studies contained AD clinical diagnostic and APOE genotype data. Homogeneous …data sets were pooled in case-control analyses. Odds ratios and 95% confidence intervals for developing AD were calculated for populations of different races and APOE genotypes. Results: The proportion of APOE genotypes and alleles differed between populations of different races. Results showed that APOE ɛ 4 was a risk factor for AD, whereas APOE ɛ 2 protected against it. The effects of APOE ɛ 4 and ɛ 2 on AD risk were distinct in various races, and they were substantially attenuated among Black people. Sub-group analysis found a higher frequency of APOE ɛ 4/ɛ 4 and lower frequency of APOE ɛ 3/ɛ 3 among early-onset AD than late-onset AD in a combined group and different races. Conclusion: Our meta-analysis suggests that the association of APOE genotypes and AD differ among races. These results enhance our understanding of APOE -related risk for AD across race backgrounds and provide new insights into precision medicine for AD. Show more

Keywords: Alzheimer’s disease, APOE genotype, race, risk

DOI: 10.3233/JAD-210549

Citation: Journal of Alzheimer's Disease, vol. 83, no. 2, pp. 897-906, 2021

Authors: Xu, Ling-Zhi | Li, Bing-Qiu | Li, Fang-Yu | Li, Ying | Qin, Wei | Zhao, Yu | Jia, Jian-Ping

Article Type: Research Article

Abstract: Background: Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia among the elderly. Excitotoxicity has been implicated as playing a dominant role in AD, especially related to the hyperactivation of excitatory neurons. Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin-dependent kinase and involved in the pathogenesis of AD, but the roles and mechanisms of DAPK1 in excitotoxicity in AD are still uncertain. Objective: We mainly explored the underlying mechanisms of DAPK1 involved in the excitotoxicity of AD and its clinical relevance. Methods: Differentiated SH-SY5Y human neuroblastoma cells, PS1 V97 L transgenic mice, and human plasma samples were used. Protein …expression was assayed by immunoblotting, and intracellular calcium and neuronal damage were analyzed by flow cytometry. Plasma DAPK1 was measured by ELISA. Results: We found that DAPK1 was activated after amyloid-β oligomers (AβOs) exposure in differentiated SH-SY5Y cells. Besides, we found the phosphorylation of GluN2B subunit at Ser1303 was increased, which contributing to excitotoxicity and Ca2+ overload in SH-SY5Y cells. Inhibiting DAPK1 activity, knockdown of DAPK1 expression, and antagonizing GluN2B subunits could effectively prevent AβOs-induced activation of GluN2B subunit, Ca2+ overload, and neuronal apoptosis. Additionally, we found that DAPK1 was elevated in the brain of AD transgenic mouse and in the plasma of AD patients. Conclusion: Our finding will help to understand the mechanism of DAPK1 in the excitotoxicity in AD and provide a reference for the diagnosis and therapy of AD. Show more

Keywords: Alzheimer’s disease, amyloid-β oligomers, death-associated protein kinase 1, excitotoxicity, GluN2B, N-methyl-D-aspartic acid receptor

DOI: 10.3233/JAD-220747

Citation: Journal of Alzheimer's Disease, vol. 91, no. 2, pp. 877-893, 2023