Abstract
Stroke is an important risk factor for dementia. Epidemiological studies have indicated a high incidence of dementia in stroke patients. There is currently no effective biomarker for the diagnosis of post-stroke dementia (PSD). D-amino acid oxidase (DAO) is a flavin-dependent enzyme widely distributed in the central nervous system. DAO oxidizes D-amino acids, a process which generates neurotoxic hydrogen peroxide and leads to neurodegeneration. This study aimed to examine post-stroke plasma DAO levels as a biomarker for PSD. In total, 53 patients with PSD, 20 post-stroke patients without dementia (PSNoD), and 71 age- and gender-matched normal controls were recruited. Cognitive function was evaluated at more than 30 days post-stroke. Plasma DAO was measured using the enzyme-linked immunosorbent assay. White matter hyperintensity (WMH), a neuroimaging biomarker of cerebral small vessel diseases, was determined by magnetic resonance imaging. We found that plasma DAO levels were independently higher in PSD subjects than in PSNoD subjects or the controls and were correlated with the WMH load in stroke patients. Using an area under the curve (AUC)/receiver operating characteristic analysis, plasma DAO levels were significantly reliable for the diagnosis of PSD. The sensitivity and specificity of the optimal cut-off value of 321 ng/ml of plasma DAO for the diagnosis of PSD were 75 and 88.7%, respectively. In conclusion, our data support that plasma DAO levels were increased in PSD patients and correlated with brain WMH, independent of age, gender, hypertension, and renal function. Plasma DAO levels may therefore aid in PSD diagnosis.
Highlights
Stroke is a risk factor for both vascular dementia and Alzheimer’s disease [1, 2]
The average post-stroke time was 3.14 ± 3.18 years with a significant difference between Post-stroke without dementia (PSNoD) and post-stroke dementia (PSD) groups when adjusted for age and gender (P = 0.046)
The average functional outcome at 30 days after stroke, rated by the Modified Rankin scale (MRS), was 0.92 ± 0.92 in stroke patients; no significant difference was found between PSNoD (0.79 ± 0.77), and PSD (1.50 ± 1.31) patients after adjusting age and gender (P = 0.08)
Summary
Stroke is a risk factor for both vascular dementia and Alzheimer’s disease [1, 2]. Functional recovery develops over the course of 26 weeks after a stroke [3], but the survivors are often left with disabilities. Limited studies have indicated that PSD involves secondary degeneration [6], including neuronal death, axonal degeneration, inflammation, and gliosis [7, 8] These secondary neurodegenerative changes result in Wallerian degeneration [9], cortical atrophy [9], white matter hyperintensities (WMHs) [9,10,11], or lacunes [9,10,11], and have been used as neuroimaging biomarkers for vascular brain injury [12] and cognitive impairment [13]. There are no effective blood biomarkers for PSD [2]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
