Your search for: 'author:("Jiang, Teng")' has returned 19 results. (0.021s) Save search

Authors: Jiang, Teng | Yu, Jin-Tai | Tan, Lan

Article Type: Review Article

Abstract: Alzheimer's disease (AD) is the most common progressive dementia in the elderly and places an enormous burden on the individual and society. Presently, the treatments for AD are only symptomatic and do not halt the progression of the disease. With the recent advances in the understanding of the pathogenesis of AD in past years, numerous therapies which could modify the disease process are under active investigation. These therapies could attenuate or even reverse the neurodegenerative process by interfering with the underlying pathogenesis including amyloid-β production, tau hyperphosphorylation, oxidative stress, inflammation, and excitotoxicity. In this review, new disease-modifying therapies which reduce …amyloid-β production, prevent tau hyperphosphorylation, and provide neuroprotective effects are described, including the results of in vitro and in vivo studies and clinical trials. Some typical therapies with disease-modifying effects have also been discussed. Show more

Keywords: Alzheimer's disease, amyloid, disease-modifying therapies, neuroprotection, tau protein

DOI: 10.3233/JAD-2012-120640

Citation: Journal of Alzheimer's Disease, vol. 31, no. 3, pp. 475-492, 2012

Authors: Wang, Si-Yu | Gong, Peng-Yu | E, Yan | Zhang, Ying-Dong | Jiang, Teng

Article Type: Review Article

Abstract: Late-onset Alzheimer’s disease (AD) accounts for most of all AD casesand is currently considered a complex disorder caused by a combination of environmental and genetic factors. As an important family member of triggering receptor expressed on myeloid cells (TREM ), TREM-like transcript 2 gene (TREML2 ) locates on human chromosome 6p21.1, a newly-identified hot zone for AD susceptibility, and encodes atransmembrane immune receptor. Emerging evidence implied a potential role of TREML2 in the susceptibility and pathogenesis of AD. Here, we review the recent literature about the association of TREML2 variants with AD risk and disease endophenotypes. Moreover, we summarize the …latest findings regarding cellular localization and biological functions of TREML2 and speculate its possible role in AD pathogenesis. In addition, we discuss future research directions of TREML2 and AD. Show more

Keywords: Alzheimer’s disease, amyloid-β, genetics, microglia, TREML2

DOI: 10.3233/JAD-200406

Citation: Journal of Alzheimer's Disease, vol. 76, no. 3, pp. 799-806, 2020

Authors: Tan, Meng-Shan | Yu, Jin-Tai | Jiang, Teng | Zhu, Xi-Chen | Guan, Hua-Shi | Tan, Lan

Article Type: Research Article

Abstract: Progressively increased proinflammatory status is a major characteristic of the aging process and associated with age-related diseases such as Alzheimer's diseases (AD). However, the regulation and role of common proinflammatory cytokines, including interleukin-12 (IL-12) and IL-23, in the aged brain are still unclear. Using the senescence-accelerated mouse prone-8 (SAMP8) model, we screened the cerebral expression of IL-12/23 in 3-, 7-, and 11-month-old mice and observed that their levels in the brain were upregulated during aging. To further examine whether the heightened activation of inflammatory cytokines may contribute to age-related brain dysfunction, we employed direct in vivo infusion of nonviral small …interfering RNA (siRNA) to knock down the common IL-12/23 signaling subunit p40 in the brain. We found that these p40-deficient mice had significantly decreased cerebral amyloid-β levels, reduced synaptic and neuronal loss, and reversed cognitive impairments. Furthermore, in vivo delivery of a neutralizing p40-specific antibody likewise ameliorated AD-associated pathology and cognitive deficits in SAMP8 mice. Thus, our data indicate that the upregulated cerebral IL-12/23 during aging is involved in age-associated brain dysfunction and point to the modulation of IL-12/23 signaling molecule p40 as a promising strategy for the development of an AD therapy. Show more

Keywords: Aging, Alzheimer's disease, amyloid-β, IL-12, IL-23, memory impairment, SAMP8

DOI: 10.3233/JAD-131148

Citation: Journal of Alzheimer's Disease, vol. 38, no. 3, pp. 633-646, 2014

Authors: Shi, Jian-Quan | Wang, Bian-Rong | Jiang, Teng | Gao, Li | Zhang, Ying-Dong | Xu, Jun

Article Type: Review Article

Abstract: As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer’s disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies …to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated. Show more

Keywords: Alzheimer’s disease, fine particulate matter, microglia, neuroinflammation, NLRP3 inflammasome

DOI: 10.3233/JAD-200359

Citation: Journal of Alzheimer's Disease, vol. 77, no. 3, pp. 923-934, 2020

Authors: Yang, Yan | Ma, Delin | Wang, Yuping | Jiang, Teng | Hu, Shuhong | Zhang, Muxun | Yu, Xuefeng | Gong, Cheng-Xin

Article Type: Research Article

Abstract: Recent studies have demonstrated that insulin plays important roles in the brain, including regulation of glucose metabolism and modulation of learning and memory. We have found dysregulation of brain insulin signaling in both Alzheimer's disease (AD) and type 2 diabetes (T2D), which correlates to hyperphosphorylation of tau, a key abnormal tau modification leading to neurofibrillary tangles. Here, we investigated tau phosphorylation and the two key components of the insulin signaling pathway, protein kinase B (AKT) and glycogen synthase kinase-3β (GSK-3β), in a rat model of T2D produced by a high protein, high glucose, and high fat diet followed by intraperitoneal …injection of streptozocin. We found tau hyperphosphorylation, decreased AKT activation, and GSK-3β over-activation in T2D rat brains. Intranasal insulin treatment for four weeks normalized AKT and GSK-3β, as well as reduced tau hyperphosphorylation in T2D rat brains, whereas four-week treatments with subcutaneous insulin had minimal effects on brain GSK-3β and tau phosphorylation. These results suggest decreased brain insulin signaling and tau hyperphosphorylation in the rat model of T2D and demonstrate the efficacy of intranasal insulin treatment to reverse these brain abnormalities. Our findings provide further mechanism by which T2D increases the risk for AD and also support the potential use of intranasal insulin for the treatment of AD. Show more

Keywords: Alzheimer's disease, AKT, GSK-3β, insulin, intranasal, tau hyperphosphorylation, type 2 diabetes

DOI: 10.3233/JAD-2012-121294

Citation: Journal of Alzheimer's Disease, vol. 33, no. 2, pp. 329-338, 2013

Authors: Tan, Lin | Yu, Jin-Tai | Tan, Meng-Shan | Liu, Qiu-Yan | Wang, Hui-Fu | Zhang, Wei | Jiang, Teng | Tan, Lan

Article Type: Research Article

Abstract: Recent findings that human serum contains stably expressed microRNAs (miRNAs) have revealed a great potential of serum miRNA signature as disease fingerprints to diagnosis. Here we used genome-wide serum miRNA expression analysis to investigate the value of serum miRNAs as biomarkers for the diagnosis of Alzheimer's disease (AD). Illumina HiSeq 2000 sequencing followed by individual quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) assays was used to test the difference in levels of serum miRNAs between 50 AD patients and 50 controls in the screening stages. The detected serum miRNAs then were validated by qRT-PCR in 158 patients and 155 controls. …MiR-98-5p, miR-885-5p, miR-483-3p, miR-342-3p, miR-191-5p, and miR-let-7d-5p displayed significantly different expression levels in AD patients compared with controls. Among the 6 miRNAs, miR-342-3p has the best sensitivity (81.5%) and specificity (70.1%) and was correlated to Mini-Mental State Examination score. This study identified six serum miRNAs that distinguish AD patients from healthy controls with high sensitivity and specificity. Serum miRNA panel (or miR-342-3p alone) may serve as a novel, noninvasive biomarker for AD. Show more

Keywords: Alzheimer's disease, biomarker, diagnosis, genome-wide sequencing, microRNA, serum

DOI: 10.3233/JAD-132144

Citation: Journal of Alzheimer's Disease, vol. 40, no. 4, pp. 1017-1027, 2014

Authors: Hu, Nan | Tan, Meng-Shan | Yu, Jin-Tai | Sun, Lei | Tan, Lin | Wang, Ying-Li | Jiang, Teng | Tan, Lan

Article Type: Short Communication

Abstract: TREM2 has been reported to be associated with Alzheimer's disease (AD). Here, we evaluated TREM2 mRNA and protein expressions in peripheral blood from AD patients and healthy controls. Higher levels of TREM2 mRNA (p = 0.002) and protein (p < 0.001) were identified in AD patients. We observed a significant correlation between TREM2 expressions and MMSE score (mRNA: r = −0.482, protein: r = −0.582; p < 0.01). According to ROC curve analysis, the diagnostic accuracy for TREM2 protein levels on monocytes was 70%, with the sensitivity and specificity 68% and 72%, respectively. Our results indicate that TREM2 might serve …as a novel noninvasive biomarker for AD diagnosis. Show more

Keywords: Alzheimer's disease, biomarker, blood, diagnosis, mRNA, plasma, protein, TREM2

DOI: 10.3233/JAD-130854

Citation: Journal of Alzheimer's Disease, vol. 38, no. 3, pp. 497-501, 2014

Authors: Fu, Xin-Xin | Wei, Bin | Cao, Hai-Ming | Duan, Rui | Deng, Yang | Lian, Hui-Wen | Zhang, Ying-Dong | Jiang, Teng

Article Type: Research Article

Abstract: Background: Alzheimer’s disease (AD) is the most common type of neurodegenerative disorder. There are few effective medications for halting the progression of AD. Telmisartan (TEL) is a widely used anti-hypertensive drug approved by FDA. Aside from treating hypertension, TEL has been revealed to provide protection against AD. However, the underlying mechanisms remain unclear. Objective: To investigate the mechanisms underlying the beneficial effects of TEL against AD. Methods: Eight-month-old APP/PS1 mice were administered with 5 mg/kg TEL once per day for 4 successive months. Nesting test, Y-maze test, and Morris water maze test were employed to assess the cognitive and executive functions. …Neuronal and synaptic markers, amyloid-β (Aβ) pathology, neuroinflammation, and oxidative stress in the brains were measured. Specifically, components involved in Aβ production and degradation pathway were analyzed to explore the mechanisms underlying the therapeutic effect of TEL against Aβ pathology. The primary microglia were used to uncover the mechanisms underlying the anti-inflammatory effects of TEL in AD. Additionally, the preventive effect of TEL against AD were investigated using 4-month-old APP/PS1 mice. Results: TEL treatment ameliorated cognitive and executive impairments, neuronal and synaptic injury, Aβ pathology, neuroinflammation, and oxidative stress in APP/PS1 mice. The favorable effects of TEL on Aβ pathology were achieved by inhibiting enzymatic Aβ production and facilitating enzymatic and autophagic Aβ degradation. Meanwhile, the anti-inflammatory effects of TEL were accomplished via microglial PPARγ /NLRP3 pathway. The administration of TEL prior to symptom onset prevented AD-related cognitive decline and neuropathologies. Conclusion: TEL represents a promising agent for AD prevention and treatment. Show more

Keywords: Alzheimer’s disease, amyloid-β pathology, autophagy, cognitive and executive impairments, neuroinflammation, neuronal and synaptic injury, NLRP3, oxidative stress, PPARγ, telmisartan

DOI: 10.3233/JAD-230133

Citation: Journal of Alzheimer's Disease, vol. 94, no. 3, pp. 919-933, 2023

Authors: Wang, Zi-Xuan | Tan, Lan | Wang, Hui-Fu | Ma, Jing | Liu, Jinyuan | Tan, Meng-Shan | Sun, Jia-Hao | Zhu, Xi-Chen | Jiang, Teng | Yu, Jin-Tai

Article Type: Research Article

Abstract: To evaluate whether iron, zinc, and copper levels in serum are disarranged in Alzheimer’s disease (AD), we performed meta-analyses of all studies on the topic published from 1984 to 2014 and contextually carried out a replication study in serum as well. Our meta-analysis results showed that serum zinc was significantly lower in AD patients. Our replication and meta-analysis results showed that serum copper was significantly higher in AD patients than in healthy controls, so our findings were consistent with the conclusions of four previously published copper meta-analyses. Even if a possible role of iron in the pathophysiology of the disease …could not be ruled out, the results of our meta-analysis showed no change of serum iron levels in AD patients, but this conclusion was not robust and requires further investigation. The meta-regression analyses revealed that in some studies, differences in serum iron levels could be due to the different mean ages, while differences in zinc levels appeared to be due to the different sex ratios. However, the effect of sex ratio on serum zinc levels in our meta-analysis is subtle and needs further confirmation. Also, diverse demographic terms and methodological approaches appeared not to explain the high heterogeneity of our copper meta-analysis. Therefore, when investigating trace elements, covariants such as age and sex have to be taken into account in the analyses. In the light of these findings, we suggest that the possible alteration of serum zinc and copper levels are involved in the pathogenesis of AD. Show more

Keywords: Alzheimer’s disease, meta-analysis, serum copper, serum iron, serum zinc

DOI: 10.3233/JAD-143108

Citation: Journal of Alzheimer's Disease, vol. 47, no. 3, pp. 565-581, 2015

Authors: Wang, Hui | Tan, Lan | Wang, Hui-Fu | Liu, Ying | Yin, Rui-Hua | Wang, Wen-Ying | Chang, Xiao-Long | Jiang, Teng | Yu, Jin-Tai

Article Type: Research Article

Abstract: Background: The application of non-invasive proton magnetic resonance spectroscopy (1 H-MRS) could potentially identify changes in cerebral metabolites in the patients with Alzheimer’s disease (AD). However, whether these metabolites can serve as biomarkers for the diagnosis of AD remains unclear. Objective: Using meta-analysis, we aimed to investigate the patterns of cerebral metabolite changes in several cerebral regions that are strongly associated with cognitive decline in AD patients. Methods: Using Hedges’ g effect size, a systematic search was performed in PubMed, Cochrane Library, Ovid, Embase, and EBSCO, and 38 studies were integrated into the final meta-analysis. Results: According to the observational …studies, N-acetyl aspartate (NAA) in AD patients was significantly reduced in the posterior cingulate (PC) (effect size (ES) =−0.924, p  <  0.005) and bilateral hippocampus (left hippocampus: ES =−1.329, p  <  0.005; right hippocampus: ES =−1.287, p  <  0.005). NAA/Cr (creatine) ratio decreased markedly in the PC (ES =−1.052, p  <  0.005). Simultaneously, significant elevated myo-inositol (mI)/Cr ratio was found not only in the PC but also in the parietal gray matter. For lack of sufficient data, we failed to elucidate the efficacy of pharmacological interventions with the metabolites changes. Conclusion: The available data indicates that NAA, mI, and the NAA/Cr ratio might be potential biomarkers of brain dysfunction in AD subjects. Choline (Cho)/Cr and mI/NAA changes might also contribute toward the diagnostic process. Thus, large, well-designed studies correlated with cerebral metabolism are needed to better estimate the cerebral extent of alterations in brain metabolite levels in AD patients. Show more

Keywords: Alzheimer’s disease, choline, creatine, glutamate and glutamine, magnetic resonance spectroscopy, meta-analysis, myo-inositol, N-acetyl aspartate

DOI: 10.3233/JAD-143225

Citation: Journal of Alzheimer's Disease, vol. 46, no. 4, pp. 1049-1070, 2015