Abstract
Cholinergic neurotransmission regulates the immune response and inhibits cytokine release after stroke. The changes in the level/activity of blood cholinesterase (ChE) in patients with post-stroke dementia (PSD) are less known. This study aimed to examine post-stroke plasma acetylcholinesterase (AChE) and butylcholinesterase (BChE) and determine whether they are biomarkers for PSD. Thirty patients with PSD, 87 post-stroke patients without dementia (PSNoD), and 117 age- and gender-matched healthy controls were recruited. Missense genetic variants AChE rs1799806 and BChE rs1803274 were genotyped. The plasma AChE level did not differ between the PSD and PSNoD groups. However, BChE levels were significantly lower in the PSD than in the PSNoD group (3300.66 ± 515.35 vs 3855.74 ± 677.60 ng/mL, respectively; p = 0.0033). The activities of total ChE, BChE, and AChE were all lower in the PSD group (19,563.33 ± 4366.03, 7650.17 ± 1912.29, 11,913.17 ± 2992.42 mU/mL, respectively) than in the PSNoD group (23,579.08 ± 5251.55, 9077.72 ± 1727.28, and 14,501.36 ± 4197.17 mU/mL, respectively). When further adjusting for age and sex, significance remained in BChE level and activity and in total ChE activity. BChE rs1803274 was associated with reduced BChE activity, while AChE rs1799806 did not influence AChE activity. The level and activity of BChE, but not of AChE, were decreased in PSD patients and may therefore aid in PSD diagnosis.
Highlights
Stroke is a major cause of dementia, especially in the elderly [1,2]
Since plasma Ach is metabolized by AChE and butylcholinesterase (BChE), the present study examined the functional activities of these two enzymes in a population of patients with chronic ischemic stroke (IS)
The inclusion criteria of stroke patients were (1) chronic stroke more than 30 days after the onset of stroke, and (2) stroke subtypes were limited to lacunar or atherothrombotic infarction to decrease the heterogeneity within the stroke groups
Summary
Stroke is a major cause of dementia, especially in the elderly [1,2]. Neuropathological studies into Alzheimer’s disease (AD) have shown that AD pathology is often concomitant with ischemic lesions in the elderly. Evidence from the Nun Study showed that lacunes increase the risk of clinical expression of cognitive impairment more than 20 times during early Braak stages that were yet sufficient to produce dementia symptoms [4]. It follows that vascular insults enhance the clinical expression of AD pathology [5]. Vascular dementia is more prevalent in men and in populations affected by cerebral small-vessel disease, including Asians, Hispanics, and Africans [6,7]
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