The Correlations Between Plasma Fibrinogen With Amyloid-Beta and Tau Levels in Patients With Alzheimer’s Disease
Open accessAbstract
Recent studies show that fibrinogen plays a role in the pathogenesis of Alzheimer’s disease (AD), which may be crucial to neurovascular damage and cognitive impairment. However, there are few clinical studies on the relationship between fibrinogen and AD. 59 11 C-PiB-PET diagnosed AD patients and 76 age- and gender-matched cognitively normal controls were included to analyze the correlation between plasma β-amyloid (Aβ) and tau levels with fibrinogen levels. 35 AD patients and 76 controls with cerebrospinal fluid (CSF) samples were included to further analyze the correlation between CSF Aβ and tau levels with fibrinogen levels. In AD patients, plasma fibrinogen levels were positively correlated with plasma Aβ40 and Aβ42 levels, and negatively correlated with CSF Aβ42 levels. Besides, fibrinogen levels were positively correlated with CSF total tau (t-tau), and phosphorylated tau-181 (p-tau) levels and positively correlated with the indicators of Aβ deposition in the brain, such as t-tau/Aβ42, p-tau/Aβ42 levels. In normal people, fibrinogen levels lack correlation with Aβ and tau levels in plasma and CSF. This study suggests that plasma fibrinogen levels are positively correlated with Aβ levels in the plasma and brain in AD patients. Fibrinogen may be involved in the pathogenesis of AD.
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Fibrinogen elevation in plasma and cerebrospinal fluid is an early biomarker of dementia risk and is associated with progression of cognitive decline in AD.
“Biomarker studies further support the notion that fibrinogen elevation in plasma and cerebrospinal fluid is an early biomarker of dementia risk and is associated with progression of cognitive decline in AD.39,45-48”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [47]
The Discussion (page unavailable) reports that cognitive function decreases as plasma fibrinogen rises in AD patients, citing earlier studies. But this study measured plasma fibrinogen—not CSF fibrinogen—and does not establish it as an early biomarker of dementia risk. The Discussion explicitly says its cross-sectional design cannot determine fibrinogen’s effect on AD progression. (LLM, conf=0.88)
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- Authors
- Fan, D.-Y., Sun, H.-L., Sun, P.-Y., Jian, J.-M., Li, W.-W., Shen, Y.-Y., Zeng, F., Wang, Y.-J., & Bu, X.-L.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Wang, Yan-Jiang
- Bu, Xian-Le
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2021-01-21
- Volume
- 14
- Pages
- 625844-625844
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC7859103
- OpenAlex
- W3121480712
- Cited by
- 27
- References
- 4
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 7 · 2023: 7 · 2022: 3 · 2021: 2
- FWCI
- 2.98
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission (cstc2020jcyj-msxmX0132)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- fibrinogen, Alzheimer's disease, amyloid-beta, tau protein, plasma biomarkers, cerebrospinal fluid biomarkers, amyloid-beta 42, phosphorylated tau 181, neurovascular injury, 11C-PiB PET, pathogenesis
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