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Published on: January 28, 2014
Biomarkers
Thanakit Pongpitakmetha1,2,3,4, Thanapoom Taweephol5, Nattanich Pornteparak6
1Department of Pharmacology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Insights
Plasma glial fibrillary acidic protein (GFAP) correlates with cerebral small vessel disease (CSVD) burden, especially in non-Alzheimer
Area of Science:
- Neurology
- Neuroimaging
- Biomarkers
Background:
- Cerebral small vessel disease (CSVD) is a primary cause of vascular cognitive impairment and dementia (VCID) and a potential co-pathology in Alzheimer's disease (AD).
- Plasma glial fibrillary acidic protein (GFAP) may indicate astrocytosis, a process implicated in both CSVD and AD.
- Understanding the relationship between CSVD biomarkers and plasma GFAP is crucial for diagnosing and managing cognitive decline.
Purpose of the Study:
- To evaluate the correlation between neuroimaging biomarkers of CSVD and plasma GFAP levels in a memory clinic cohort.
- To investigate whether this correlation differs between patients with and without Alzheimer's disease (AD).
- To explore the influence of AD biomarkers on the relationship between CSVD and plasma GFAP.
Main Methods:
- Collected clinical information and plasma biomarkers from 114 participants in memory clinics.
- Categorized patients into AD and non-AD groups using established criteria (CSF Aβ 42/p-tau181 ratio or Aβ PET).
- Assessed CSVD using MRI-based STRIVE-2 criteria and calculated a composite total CSVD score; analyzed correlations using non-parametric statistics.
Main Results:
- A significant positive correlation was found between the total CSVD score and plasma GFAP in the overall cohort and the non-AD group.
- This correlation strengthened considerably in the whole cohort after adjusting for plasma p-tau 217, a key AD biomarker.
- Specific neuroimaging biomarkers of CSVD showed a positive correlation with plasma GFAP, though not universally across all markers.
Conclusions:
- The correlation between CSVD burden and plasma GFAP is stronger in individuals without AD compared to those with AD.
- Adjusting for AD biomarkers like p-tau 217 enhances the observed correlation between CSVD score and plasma GFAP.
- Plasma GFAP alone may have limitations in reflecting CSVD burden in AD patients due to overlapping pathological mechanisms; further research into other fluid biomarkers for VCID is recommended.
Background:
Cerebral small vessel disease (CSVD) is one of the leading causes of vascular cognitive impairment and dementia (VCID) in the aging population. It may also contribute to a faster rate of clinical deterioration in Alzheimer's disease (AD) as a co-pathology. Plasma glial fibrillary acidic protein (GFAP) may be elevated due to astrocytosis in either CSVD or AD pathogenesis. This study evaluates the correlation between CSVD neuroimaging biomarkers and plasma GFAP in a memory clinic cohort.
Methods:
The clinical information and plasma biomarkers were collected from memory clinic cohorts. Patients were categorized into AD and non-AD groups based on either an abnormal cerebrospinal fluid Amyloid beta (Aβ) 42/p-tau181 ratio, or a positive Aβ Positron Emission Topography. Magnetic resonance imaging (MRI) was independently rated by the two trained investigators using STRIVE-2 criteria (Duering M, 2023). The validated composite total CSVD score (Staals J, 2014) ranging from 0-4 was calculated. The non-parametric statistical analysis was applied to analyze.
Results:
A total of 114 participants were enrolled. Clinical information, laboratory test results, and neuroimaging biomarkers were compared between AD and non-AD groups, as shown in Table 1. A positive correlation exists between the total CSVD score and plasma GFAP in the whole and non-AD cohort (Spearman rho = 0.29, p-value 0.002). After the adjustment for plasma p-tau 217, the notable positive correlation between total CSVD score and plasma GFAP in the whole cohort (Spearman rho = 0.56, p-value < 0.001) is observed as demonstrated in visualized correlation plots in Figure 1. The results of Spearman's correlation and the Wilcoxon rank sum test between plasma GFAP and each neuroimaging biomarker are summarized in Table 2, where only certain neuroimaging biomarkers demonstrated a positive correlation.
Conclusion:
The total CSVD score and plasma GFAP showed a stronger positive correlation in the non-AD group than in the AD group. After adjusting for p-tau 217, an AD biomarker, the correlation between total CSVD score and plasma GFAP became stronger. These findings suggest that plasma GFAP alone may have limitations in assessing CSVD burden in AD due to shared mechanisms and biomarkers. Further validation of other potential VCID fluid biomarkers is warranted.
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