Elevated Serum Amyloid A Is Associated With Cognitive Impairment in Ischemic Stroke Patients

So you described something, but DID NOTHING USEFUL THAT WILL HELP STROKE PATIENTS RECOVER. Why the fuck are you in stroke anyway?

 

Elevated Serum Amyloid A Is Associated With Cognitive Impairment in Ischemic Stroke Patients

Yun Zhang^1*, Yue Feng², Jiacai Zuo¹, Jian Shi¹, Shanshan Zhang¹, Yao Yang¹, Shu Xie¹ and Zhonglun Chen^1*

• ¹Department of Neurology, Mianyang Central Hospital, Mianyang, China
• ²Department of Medical Laboratory, Mianyang Central Hospital, Mianyang, China

Background and Purpose: The impact of serum amyloid A on cognitive impairment after ischemic stroke is unclear. We aimed to investigate the association between serum amyloid A (SAA) levels and post-stroke cognitive impairment (PSCI) at 3 months after ischemic stroke.

Methods: One hundred and ninety-eight patients were enrolled prospectively from June 2020 to April 2021. The SAA concentrations were measured using a commercially available enzyme-linked immunosorbent assay kit after admission. Cognitive function was assessed using the Montreal Cognitive Assessment score at 3 months after the symptom onset. We defined a Montreal Cognitive Assessment score <25 as cognitive impairment.

Results: During 3-month follow-up, 80 patients (40.4%) were diagnosed as having PSCI. As compared with patients with cognitively normal ischemic stroke, those with PSCI were older, more likely to have diabetes and white matter lesions, and had a higher baseline National Institutes of Health stroke score and SAA levels. After adjustment for age, the National Institutes of Health stroke score and other covariates, the OR for the highest quartile of SAA compared with the lowest quartile was 5.72 (95% CI, 2.17–15.04, P = 0.001) for PSCI. Also, ordinal logistic regression analysis showed that higher SAA concentrations were associated with increased risk of PSCI severity (OR, 4.31; 95% CI, 1.81–10.33, P = 0.001). Similar results were found when the SAA levels were analyzed as a continuous variable.

Conclusions: This present study demonstrated that increased SAA levels might be associated with PSCI at 3 months after ischemic stroke.

Introduction

Stroke is one of the major devastating diseases with high rates of mortality and long-term disability (1, 2). Post-stroke cognitive impairment (PSCI) is a common consequence of stroke affecting as high as 80% of stroke survivors (3, 4). It may reduce medication adherence and induce a poor functional outcome after stroke (5–7). Also, it has been reported that PSCI may be associated with increased risk of mortality and recurrent stroke (6, 8, 9). To date, associated factors and underlying pathophysiology of PSCI are not well-determined, which may be a contributing factor to why the mortality and long-term disability risk in ischemic stroke survivors remained high. Therefore, determining new prognostic markers is of vital importance for continuously improving the prognosis of stroke and providing insight into underlying pathophysiology of PSCI.

Serum amyloid A is one of highly conserved acute-phase proteins, which are involved in the chemotactic recruitment of inflammatory cells (10). Serum amyloid A (SAA) concentrations rise rapidly when the body is infected, wounded, or inflamed. The production of acute-phase SAA is triggered by proinflammatory cytokines, such as interleukin-1, interleukin-6, and transforming growth factor-β. Recently, it has been proved that SAA may play an important role in various central nervous system diseases (10, 11). SAA has been found to be substantially associated with the severity of senile early cognitive impairment (12). In a recent experimental study, cerebral ischemia could induce a systemic inflammatory response through SAA that might contribute to the pathological outcomes (13). Also, previous studies reported that SAA levels were significantly higher in patients with ischemic stroke who died compared with those who survived and were independently associated with early death, after adjusting for various confounders (14). However, in the cognitive impairment after ischemic stroke, the role of SAA has not yet been assessed. In this prospective cohort study, we aim to assess whether SAA levels could be an effective predictor of PSCI during a 3-month follow-up period.

More at link.