Fibrinogen and risk of dementia: A systematic review and meta-analysis

Zhou, Zhike; Liang, Yifan; Zhang, Xiaoqian; Xu, Junjie; Lin, Jueying; Zhang, Rongwei; Kang, Kexin; Qu, Huiling; Zhao, Chuansheng; Zhao, Mei

doi:10.1016/j.neubiorev.2020.02.022

Cited by 13 publications

(10 citation statements)

References 42 publications

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“…In line with these results, a prospective population‐based study that measured plasma fibrinogen levels in 2835 individuals longitudinally found that high fibrinogen levels were associated with increased risk of AD and dementia 90 . Furthermore, a meta‐analysis involving 3649 patients with dementia had significantly higher plasma fibrinogen levels than nondemented individuals 91 …”

Section: Fibrinogen: a Significant Contributor To Ad Pathogenesismentioning

confidence: 63%

“…90 Furthermore, a meta-analysis involving 3649 patients with dementia had significantly higher plasma fibrinogen levels than nondemented individuals. 91 It is important to note that some Aβ mutations that are associated with EOAD, particularly the Dutch (E22Q) and Iowa (D23 N) mutations, increase Aβ's toxicity as well as its vascular deposition. 55,[92][93][94][95][96][97] More specifically, the Dutch and Iowa Aβ mutations have a 50-fold higher binding affinity for fibrinogen.…”

Section: Fib Rinog En: a S Ig Nific Ant Contributor To Ad Pathog Ene S Ismentioning

confidence: 99%

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The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy

Singh

Badimon

Chen

et al. 2021

Research and Practice in Thrombosis and Haemostasis

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Alzheimer's disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. Extracellular beta‐amyloid (Aβ) plaques and neurofibrillary tau tangles are classical hallmarks of AD pathology and thus are the prime targets for AD therapeutics. However, approaches to slow or stop AD progression and dementia by reducing Aβ production, neutralizing toxic Aβ aggregates, or inhibiting tau aggregation have been largely unsuccessful in clinical trials. The contribution of dysregulated vascular components and inflammation is evident in AD pathology. Vascular changes are detectable early in AD progression, so treatment of vascular defects along with anti‐Aβ/tau therapy could be a successful combination therapeutic strategy for this disease. Here, we explain how vascular dysfunction mechanistically contributes to thrombosis as well as inflammation and neurodegeneration in AD pathogenesis. This review provides evidence that addressing vascular dysfunction in people with AD could be a promising therapeutic strategy.

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Section: Fibrinogen: a Significant Contributor To Ad Pathogenesismentioning

confidence: 63%

Section: Fib Rinog En: a S Ig Nific Ant Contributor To Ad Pathog Ene S Ismentioning

confidence: 99%

The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy

Singh

Badimon

Chen

et al. 2021

Research and Practice in Thrombosis and Haemostasis

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“…Dementia is a group of acquired clinical syndromes characterized by the progressive decline in cognition along with psychiatric and behavioral alterations of differing extents (Tari et al, 2019;Zhou et al, 2020). More than 50 million people worldwide suffer from the overload burden of finance due to this clinical entity, a number that is alarmingly expected to triple by 2050 (Kivipelto et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Serum Uric Acid and the Risk of Dementia: A Systematic Review and Meta-Analysis

Zhou

Zhong

Liang

et al. 2021

Front. Aging Neurosci.

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Background: This meta-analysis aimed to evaluate the relationship between serum uric acid (UA) and the risk of dementia and its subtypes.Methods: Embase, PubMed, and Web of Science were searched from inception to July 2020. Random-effect models were employed to analyze the standard mean difference (SMD) with the corresponding 95% confidence intervals (CI).Results: Twenty-three eligible studies involving 5,575 participants were identified. The overall results showed lower levels of UA in dementia relative to non-dementia controls [SMD = −0.32 (−0.64; −0.01) p = 0.04]. The subgroup analysis of the type of dementia demonstrated a significant association of UA with Alzheimer's disease (AD) [SMD = −0.58 (−1.02; −0.15) p = 0.009] and Parkinson's disease with dementia (PDD) [SMD = −0.33 (−0.52; −0.14) p = 0.001] but not with vascular dementia (VaD). The stratification analysis of the concentrations of UA revealed that the UA quartile 1–2 was negatively correlated with dementia and neurodegenerative subtypes (p < 0.05), whereas a positive correlation of UA quartile 4 with dementia was noted (p = 0.028). Additionally, the meta-regression analysis on confounders showed that not age, body mass index, diabetes mellitus, hypertension, or smoking but education (p = 0.003) exerted an influence of the UA in the risk estimate of dementia.Conclusions: Low concentrations of UA (< 292 μmol/L or 4.91 mg/dL) is a potential risk factor for AD and PDD but not for VaD. The mechanism of different concentrations of the UA in dementia needs to be confirmed through further investigation.

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“…Alzheimer's disease (AD), referring to an irreversible neurodegenerative disorder, is manifested in cognitive decline, along with behavioral and psychiatric abnormalities of varying extent [1,2]. The core hallmarks of AD comprise intracellular hyperphosphorylated tau and extracellular amyloidbeta (Aβ) plaques, which progressively deteriorate with loss of neurons and synaptic elements [3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of PIK3CB Involved in Alzheimer’s Disease via Apoptosis, Axon Guidance, and FoxO Signaling Pathway

Zhou

Bai

Zhong

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. To investigate the molecular function of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PIK3CB) underlying Alzheimer’s disease (AD). Methods. RNA sequencing data were used to filtrate differentially expressed genes (DEGs) in AD/nondementia control and PIK3CB-low/high groups. An unbiased coexpression network was established to evaluate module-trait relationships by using weight gene correlation network analysis (WGCNA). Global regulatory network was constructed to predict the protein-protein interaction. Further cross-talking pathways of PIK3CB were identified by functional enrichment analysis. Results. The mean expression of PIK3CB in AD patients was significantly lower than those in nondementia controls. We identified 2,385 DEGs from 16,790 background genes in AD/control and PIK3CB-low/high groups. Five coexpression modules were established using WGCNA, which participated in apoptosis, axon guidance, long-term potentiation (LTP), regulation of actin cytoskeleton, synaptic vesicle cycle, FoxO, mitogen-activated protein kinase (MAPK), and vascular endothelial growth factor (VEGF) signaling pathways. DEGs with strong relation to AD and low PIK3CB expression were extracted to construct a global regulatory network, in which cross-talking pathways of PIK3CB were identified, such as apoptosis, axon guidance, and FoxO signaling pathway. The occurrence of AD could be accurately predicted by low PIK3CB based on the area under the curve of 71.7%. Conclusions. These findings highlight downregulated PIK3CB as a potential causative factor of AD, possibly mediated via apoptosis, axon guidance, and FoxO signaling pathway.

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Fibrinogen and risk of dementia: A systematic review and meta-analysis

Cited by 13 publications

References 42 publications

The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy

The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy

Serum Uric Acid and the Risk of Dementia: A Systematic Review and Meta-Analysis

Downregulation of PIK3CB Involved in Alzheimer’s Disease via Apoptosis, Axon Guidance, and FoxO Signaling Pathway

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