Background/Purpose: Previous studies documented a close relationship between stroke and dementia. Increases in cerebrospinal fluid or plasma β-amyloids (Aβ) and tau proteins have been noted in patients with Alzheimer’s dementia, but whether levels of Aβ and tau proteins showed difference in stroke patients with or without vascular cognitive impairment (VCI) remained uncertain. Our study aimed to investigate the associations of plasma Aβ and tau proteins and the development of VCI in stroke patients.
Methods: This cross-sectional study recruited patients with chronic stroke and controls free of stroke and dementia at an university medical center stroke clinic. VCI was defined as the scale of Clinical Dementia Ranking (CDR) ≥1. The levels of β-amyloids 42 (Aβ-42) and tau protein in the blood were analyzed using immunomagnetic reduction (IMR). One-way analysis of variance was used to compare the differences of measured proteins between the 3 groups.
Results: This study included 26 controls (mean age 67.3±7.3 years, 30.8% male), 27 stroke patients without VCI (mean age 70.7±6.9 years, 60.7% male) and 34 stroke patients with VCI (mean age 78.3±5.3 years, 45.5% male). Plasma levels of tau and Aβ-42 were both significantly higher in stroke patients (with or without VCI) than in controls (Figure 1). However, Aβ-42, but not tau levels were significantly higher in stroke patients with VCI than those without VCI (17.6±2.6 versus 15.4±1.8 pg/ml, p< 0.01). Furthermore, after adjustment for age, sex, and vascular risk factors including diabetes mellitus and hypertension, plasma levels of Aβ-42 remained significantly higher in stroke patients with VCI than those without VCI (p= 0.02).
Conclusion: Not only a potential biomarker for stroke patients with VCI, our finding also suggested the pathophysiological role of Aβ-42 in the development of VCI in stroke patients.