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4. MTHFR gene A1298C (rs1801131) polymorphism and its correlations with cerebrospinal fluid biomarkers, cognitive level, and brain structure changes in patients with Alzheimer’s disease

Author

MA Yuju, HUANG Liangyu, CHEN Jiaru, TAN Lan

Subjects
alzheimer disease, methylenetetrahydrofolate reductase (nadph2), polymorphism,single nucleotide, folic acid, homocysteine, cerebrospinal fluid, amyloid beta-peptides, cognition disorders, Medicine
Abstract

Objective To investigate the relationship of A1298C (rs1801131) polymorphism in the MTHFR gene encoding methylenetetrahydrofolate reductase with the cerebrospinal fluid β-amyloid 1-42 subtype (Aβ1-42) level, cognitive level, and brain structure changes in patients with Alzheimer’s disease (AD). Methods A total of 1 271 subjects who met the inclusion criteria in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database were selected. A multivariable linear regression model was used to analyze the relationship of MTHFR gene A1298C (rs1801131) polymorphism with cerebrospinal fluid Aβ1-42 level, cognitive level, and brain structure changes in AD patients. A mediation model was used to analyze the role of cerebrospinal fluid Aβ1-42 level in mediating the relationship between MTHFR gene A1298C (rs1801131) polymorphism and cognitive level. Results Multivariable linear regression model analysis showed that A1298C-C allele was negatively correlated with the level of Aβ1-42 in cerebrospinal fluid, hippocampal volume, and cognitive level (β=-0.121--0.084,t=-3.308--1.953,P more...

Published
2024
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27. ASSOCIATION OF TMEM106B GENE POLYMORPHISMS WITH THE PATHOGENESIS OF ALZHEIMER’S DISEASE

Author

XIE Tingfei, TAN Lan

Subjects
lysosome-associated membrane glycoproteins, polymorphism, single nucleotide, alzheimer disease, amyloid beta-peptides, tau proteins, Medicine
Abstract

Objective To investigate the possible role of TMEM106B in Alzheimer’s disease (AD). Methods A total of 308 subjects who were included in the Alzheimer’s disease Neuroimaging Initiative cohort study and underwent TMEM106B rs1990622 genotyping, cerebrospinal fluid (CSF) core protein detection, and neuroimaging measurements were enrolled, and according to the level of CSF β amyloid protein 42 (Aβ1-42), they were divided into AD pathological group and non-AD pathological group. Related data were collected, including age, sex, years of education, genotype, levels of CSF core proteins [Aβ1-42, total tau (T-tau), and phosphorylated tau (P-tau)], and neuroimaging indicators [MRI results of the hippocampus, the entorhinal cortex, and the medial temporal lobe and standard intake value (SUV) on fluorodeoxyglucose positron emission computed tomography (FDG-PET)]. The chi-square test or the t-test was used for comparison of the above indices between the two groups, and the multivariate linear regression model was used to analyze the association of TMEM106B rs1990622 polymorphism with the key phenotype of AD. Results A pairwise comparison showed that there were significant differences between the AD pathological group and the non-AD pathological group in the levels of Aβ1-42, T-tau, and p-tau, the proportion of patients carrying APOE ɛ4, FGG-PET SUV, and the volume of various brain regions (hippocampus, medial temporal lobe, and entorhinal cortex) (t=-6.137-50.792,P more...

Published
2023
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28. Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer’s amyloid, tau and FDG PET status

Author

Shen, Xue-Ning, Huang, Yu-Yuan, Chen, Shi-Dong, Guo, Yu, Tan, Lan, Dong, Qiang, and Yu, Jin-Tai

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Clinical Research, Aging, Prevention, Dementia, Neurosciences, Alzheimer's Disease, Brain Disorders, Biomedical Imaging, 4.1 Discovery and preclinical testing of markers and technologies, 4.2 Evaluation of markers and technologies, 2.1 Biological and endogenous factors, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Fluorodeoxyglucose F18, Humans, tau Proteins, Alzheimer’s Disease Neuroimaging Initiative, Public Health and Health Services, Psychology, Clinical sciences, Biological psychology
Abstract

Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. We aimed to evaluate whether it could serve as a marker for Alzheimer's pathology in the brain. A total of 1189 participants with plasma p-tau181 and PET data of amyloid, tau or FDG PET were included from ADNI. Cross-sectional relationships of plasma p-tau181 with PET biomarkers were tested. Longitudinally, we further investigated whether different p-tau181 levels at baseline predicted different progression of Alzheimer's pathological changes in the brain. We found plasma p-tau181 significantly correlated with brain amyloid (Spearman ρ = 0.45, P 18.85 pg/ml) at baseline had a higher risk of pathological progression in brain amyloid (HR: 2.32, 95%CI 1.32-4.08) and FDG PET (3.21, 95%CI 2.06-5.01) status. Plasma p-tau181 may be a sensitive screening test for detecting brain pathologies, and serve as a predictive biomarker for Alzheimer's pathophysiology. more...

Published
2021

29. Staging tau pathology with tau PET in Alzheimer’s disease: a longitudinal study

Author

Chen, Shi-Dong, Lu, Jia-Ying, Li, Hong-Qi, Yang, Yu-Xiang, Jiang, Jie-Hui, Cui, Mei, Zuo, Chuan-Tao, Tan, Lan, Dong, Qiang, and Yu, Jin-Tai

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Dementia, Biomedical Imaging, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease, Brain Disorders, Clinical Research, Aging, Acquired Cognitive Impairment, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, Neurological, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Cognitive Dysfunction, Female, Humans, Longitudinal Studies, Male, Positron-Emission Tomography, tau Proteins, Alzheimer’s Disease Neuroimaging Initiative, Public Health and Health Services, Clinical sciences, Biological psychology
Abstract

A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). However, it cannot characterize the hierarchy spreading pattern of tau pathology. To reflect in vivo tau progression using biomarker, we constructed a refined topographic 18F-AV-1451 tau PET staging scheme with longitudinal clinical validation. Seven hundred and thirty-four participants with baseline 18F-AV-1451 tau PET (baseline age 73.9 ± 7.7 years, 375 female) were stratified into five stages by a topographic PET staging scheme. Cognitive trajectories and clinical progression were compared across stages with or without further dichotomy of amyloid status, using linear mixed-effect models and Cox proportional hazard models. Significant cognitive decline was first observed in stage 1 when tau levels only increased in transentorhinal regions. Rates of cognitive decline and clinical progression accelerated from stage 2 to stage 3 and stage 4. Higher stages were also associated with greater CSF phosphorylated tau and total tau concentrations from stage 1. Abnormal tau accumulation did not appear with normal β-amyloid in neocortical regions but prompt cognitive decline by interacting with β-amyloid in temporal regions. Highly accumulated tau in temporal regions independently led to cognitive deterioration. Topographic PET staging scheme have potentials in early diagnosis, predicting disease progression, and studying disease mechanism. Characteristic tau spreading pattern in Alzheimer's disease could be illustrated with biomarker measurement under NIA-AA framework. Clinical-neuroimaging-neuropathological studies in other cohorts are needed to validate these findings. more...

Published
2021

38. Indobufen versus aspirin in patients with acute ischaemic stroke in China (INSURE): a randomised, double-blind, double-dummy, active control, non-inferiority trial

Author

Wang, Yongjun, Wang, Yanxia, Wang, Cunrui, Han, Yazhou, Yu, Ming, Yang, Hongqin, Zou, Guoping, Wu, Aisheng, Zhang, Guiru, Zhang, Ping, Yan, Mingzong, Zhang, Jia, Zhao, Jingyan, Zhang, Huitian, Qi, Qinde, Zhang, Jianling, Zhu, Zhishan, Zhao, Jinguo, Fan, Wenfeng, Li, Xueli, Chang, Liguo, Tan, Lan, Zhao, Liang, Xue, Yanzhong, Liu, Peiru, Ju, Xiaohua, Zhang, Zuowen, Li, Linwen, Wei, Feng, Yang, Lixia, Li, Xuemei, Zheng, Zhixiong, Liang, Hui, Wei, Yan, Zhang, Ming, Wang, Ting, Yang, Jianbo, Liu, Qing, Huang, Panbing, Tan, Guojun, Chen, Yongming, Zhou, Jin, An, Zhongping, Li, Chunlei, Chen, Guohua, Zhu, Runxiu, Sun, Xin, Liu, Yong, Zhang, Mei, Zhuo, Yanguang, Meng, Fanwen, Zhu, Hui, Li, Kebo, Zhang, Wei, Chai, Xiangting, Deng, Ke, Li, Jianhua, Cai, Zhiyou, Jin, Hailian, Li, Bo, Zhang, Xiaomei, Ge, Beihai, Hu, Wei, Jiao, Zhen, Zhong, Lianmei, Ren, Lijie, Li, Xinyi, Wu, Songdi, Wan, Yinguo, Zhang, Jinghua, Ma, Xiaoyan, Hu, Jizheng, Zhang, Ge, Zheng, Chunling, Xu, Jun, Zou, YuAn, Huang, Xuerong, Duan, Zhihui, Li, Changxin, Zhang, Qingxiu, Song, Xiaoming, Jia, Zhengchang, Wang, Chun, Shao, Peining, Teng, Jijun, Bao, Hua, Chen, Yangkun, Wei, Yunfei, Zhang, Xu, Meng, Xisi, Li, Guangning, Feng, Yefang, Pan, Pengke, Zhuang, Aixia, Dong, Qiang, Chen, Xiaofei, Zhou, Yanhua, Tang, Jun, An, Hongwei, You, Shihao, Tang, Yanyan, Zhang, Guilian, Li, Hongyan, Guo, Miao, Yu, Chunlei, Li, Ying, Liu, Haichao, Liang, Pengfei, Kang, Guangming, Sun, Huijie, Che, Yu, Tang, Juan, Li, Dandan, Feng, Xiaopeng, Geng, Yu, Liu, Bin, Wang, Huibing, Shen, Ping, Zhu, Huaiping, Li, Farong, Zhang, Lifang, Cao, Minghua, You, Yong, Cui, Guiyun, Gu, Jun, Li, Haitao, Zhang, Xiangfeng, Liu, Xiaojun, Chen, Houqin, Zhang, Yuehua, Zhao, Hongnian, Liang, Ke, Zhi, Rui, Ma, Ling, Wu, Yuanhua, Geng, Yalan, Sun, Ping, Zhong, Bing, Li, Dongxue, Jiao, Jingya, Hao, Yanlei, Li, Guozhong, Su, Shaohua, Ju, Weiping, Min, Lianqiu, Guo, Liyan, Shangguan, Yafei, Tai, Yingdong, Xing, Ying, Chang, Hongshan, Chen, Wenya, Tang, Hongtao, Huang, Shuchun, Fang, Jingxian, Yu, Donghui, Zhao, Hailong, Xu, Lei, Wu, Aimei, Wan, Hebin, Wang, Hongliang, Shen, Zhihui, Zhang, Qing, Wang, Qian, Pan, Yuesong, Meng, Xia, Yuan, Baoshi, Johnston, S Claiborne, Li, Hao, Bath, Philip M, Xu, Anding, Jing, Jing, Lin, Jinxi, Jiang, Yong, Xie, Xuewei, Jin, Aoming, Suo, Yue, Xiong, Yunyun, Li, Zixiao, Wang, Yilong, Zhao, Xingquan, and Liu, Liping more...

Published
2023
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39. Prioritization of Drug Targets for Neurodegenerative Diseases by Integrating Genetic and Proteomic Data From Brain and Blood

Author

Ferrari, Raffaele, Hernandez, Dena G., Nalls, Michael A., Rohrer, Jonathan D., Ramasamy, Adaikalavan, Kwok, John B.J., Dobson-Stone, Carol, Brooks, William S., Schofield, Peter R., Halliday, Glenda M., Hodges, John R., Piguet, Olivier, Bartley, Lauren, Thompson, Elizabeth, Haan, Eric, Hernández, Isabel, Ruiz, Agustín, Boada, Mercè, Borroni, Barbara, Padovani, Alessandro, Cruchaga, Carlos, Cairns, Nigel J., Benussi, Luisa, Binetti, Giuliano, Ghidoni, Roberta, Forloni, Gianluigi, Galimberti, Daniela, Fenoglio, Chiara, Serpente, Maria, Scarpini, Elio, Clarimón, Jordi, Lleó, Alberto, Blesa, Rafael, Waldö, Maria Landqvist, Nilsson, Karin, Nilsson, Christer, Mackenzie, Ian R.A., Hsiung, Ging-Yuek R., Mann, David M.A., Grafman, Jordan, Morris, Christopher M., Attems, Johannes, Griffiths, Timothy D., McKeith, Ian G., Thomas, Alan J., Pietrini, P., Huey, Edward D., Wassermann, Eric M., Baborie, Atik, Jaros, Evelyn, Tierney, Michael C., Pastor, Pau, Razquin, Cristina, Ortega-Cubero, Sara, Alonso, Elena, Perneczky, Robert, Diehl-Schmid, Janine, Alexopoulos, Panagiotis, Kurz, Alexander, Rainero, Innocenzo, Rubino, Elisa, Pinessi, Lorenzo, Rogaeva, Ekaterina, St. George-Hyslop, Peter, Rossi, Giacomina, Tagliavini, Fabrizio, Giaccone, Giorgio, Rowe, James B., Schlachetzki, Johannes C.M., Uphill, James, Collinge, John, Mead, Simon, Danek, Adrian, Van Deerlin, Vivianna M., Grossman, Murray, Trojanowski, John Q., van der Zee, Julie, Deschamps, William, Van Langenhove, Tim, Cruts, Marc, Van Broeckhoven, Christine, Cappa, Stefano F., Le Ber, Isabelle, Hannequin, Didier, Golfier, Véronique, Vercelletto, Martine, Brice, Alexis, Nacmias, Benedetta, Sorbi, Sandro, Bagnoli, Silvia, Piaceri, Irene, Nielsen, Jørgen E., Hjermind, Lena E., Riemenschneider, Matthias, Mayhaus, Manuel, Ibach, Bernd, Gasparoni, Gilles, Pichler, Sabrina, Gu, Wei, Rossor, Martin N., Fox, Nick C., Warren, Jason D., Spillantini, Maria Grazia, Morris, Huw R., Rizzu, Patrizia, Heutink, Peter, Snowden, Julie S., Rollinson, Sara, Richardson, Anna, Gerhard, Alexander, Bruni, Amalia C., Maletta, Raffaele, Frangipane, Francesca, Cupidi, Chiara, Bernardi, Livia, Anfossi, Maria, Gallo, Maura, Conidi, Maria Elena, Smirne, Nicoletta, Rademakers, Rosa, Baker, Matt, Dickson, Dennis W., Graff-Radford, Neill R., Petersen, Ronald C., Knopman, David, Josephs, Keith A., Boeve, Bradley F., Parisi, Joseph E., Seeley, William W., Miller, Bruce L., Karydas, Anna M., Rosen, Howard, van Swieten, John C., Dopper, Elise G.P., Seelaar, Harro, Pijnenburg, Yolande A.L., Scheltens, Philip, Logroscino, Giancarlo, Capozzo, Rosa, Novelli, Valeria, Puca, Annibale A., Franceschi, Massimo, Postiglione, Alfredo, Milan, Graziella, Sorrentino, Paolo, Kristiansen, Mark, Chiang, Huei-Hsin, Graff, Caroline, Pasquier, Florence, Rollin, Adeline, Deramecourt, Vincent, Lebert, Florence, Kapogiannis, Dimitrios, Ferrucci, Luigi, Pickering-Brown, Stuart, Singleton, Andrew B., Hardy, John, Momeni, Parastoo, Ge, Yi-Jun, Ou, Ya-Nan, Deng, Yue-Ting, Wu, Bang-Sheng, Yang, Liu, Zhang, Ya-Ru, Chen, Shi-Dong, Huang, Yu-Yuan, Dong, Qiang, Tan, Lan, and Yu, Jin-Tai more...

Published
2023
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50. Frailty increases the risk of Alzheimer's disease in non-demented individuals: A longitudinal cohort study.

Author

Sheng, Ze-Hu, Liu, Jia-Yao, Ma, Jun-Yi, Mi, Yin-Chu, Wang, Hao, Guo, Fan, Ma, Ling-Zhi, and Tan, Lan

Abstract

Background: Frailty, which is considered a potential modifiable risk factor for dementia, continues to generate debate when it comes to Alzheimer's disease (AD). Furthermore, the underlying pathological mechanisms linking frailty to AD remain uncertain. Objective: We aimed to investigate the relationship between frailty and the risk of AD while elucidating the connections between frailty, AD biomarkers, and cognitive function. Methods: Total of 829 non-frail (261 robust, 568 pre-frail) and 94 frail individuals from the Alzheimer's Disease Neuroimaging Initiative database were recruited. Kaplan–Meier analysis and Cox regression assessed AD risk across diverse frail statuses in 923 non-demented individuals. Multiple linear regression, mixed effects models and causal mediation analyses bootstrapped 10,000 iterations were conducted to examined underlying associations. Results: The frail group had a 67.7% increased risk of AD than non-frail group (HR = 1.677; 95%CI, 1.179–2.385; p = 0.004), a 61.8% increased risk of AD than pre-frail group (HR = 1.618; 95%CI, 1.131–2.316; p = 0.009) and a far higher risk of AD than robust group (HR = 2.011; 95%CI, 1.263–3.202; p = 0.003). Frailty was associated with cognitive decline (global cognition, memory and executive function), whole brain and hippocampus atrophy, and ventricle dilation. Higher frail degree predicted faster cognitive decline, brain atrophy and ventricle dilation. Frailty's association with cognition was partially mediated by volume of whole brain (29.54%–30.17% of total effect), hippocampus (18.21%–24.55% of total effect), and ventricle (baseline, 7.62%–10.87% of total effect; change rate, 13.30%–24.33% of total effect). Conclusions: Frailty as a potential risk factor for AD, further mechanisms investigation is warranted; mitigating frailty could potentially contribute to AD prevention. [ABSTRACT FROM AUTHOR] more...

Published
2025
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