Early neutrophil-to-lymphocyte ratio is a prognostic marker in acute minor stroke or transient ischemic attack.

Intravenous injection of alteplase is recommended for patients with minor disabling and not non-disabling ischemic stroke symptoms within 4.5 h of ischemic stroke symptom onset. However, it is hard for clinicians to distinguish which type of minor ischemic stroke is disabled at an early stage. In this study, we aimed to demonstrate early neutrophil-to-lymphocyte ratio is a prognostic marker in acute minor stroke or transient ischemic attack. 196 patients diagnosed with acute minor stroke or transient ischemic attack within 24 h of symptom onset were enrolled. Patients were divided into three groups according to the neutrophil-to-lymphocyte ratio value (< 2, 2-3, > 3). Clinical, neuroradiological, laboratory and follow-up data were collected from electronic database. Functional outcome was assessed by modified Rankin Scale. Neutrophil-to-lymphocyte ratio associated with functional outcome of 90 days was evaluated by logistic regression analysis, and we used receiver operating characteristic curve analysis to detect the overall predictive accuracy of this marker. Early neutrophil-to-lymphocyte ratio was associated with an increased risk of short-term functional outcome (OR 4.502, 95% CI 1.533-13.046, P = 0.006). The optimal cutoff value of neutrophil-to-lymphocyte ratio for prediction of short-term unfavorable outcome was 2.94 with a sensitivity of 69.6% and a specificity of 77.1% (area under the curve: 0.767, 95% CI 0.691-0.843). Early neutrophil-to-lymphocyte ratio is associated with short-term unfavorable functional outcome in patients with acute minor stroke or transient ischemic attack. Early neutrophil-to-lymphocyte ratio is beneficial for clinicians to distinguish minor disabling ischemic stroke at an early stage.

MiR-340 Reduces the Accumulation of Amyloid-ß Through Targeting BACE1 (ß-site Amyloid Precursor Protein Cleaving Enzyme 1) in Alzheimer's Disease.

BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease, and the accumulation of amyloid-ß is the initial process in AD. MicroRNAs (miRNAs) are widely known as key regulators of the accumulation of amyloid-ß in AD. This study analyzed the potential effects and possible internal mechanisms of miR-340 on AD. METHODS: The expression of miR-340 in senescence-accelerated mouse prone-8 (SAMP8) mouse and senescence-accelerated mice/resistant-1 (SAMR1) mouse was evaluated by qRT-PCR (quantitative real-time polymerase chain reaction). The expression of ß-site amyloid precursor protein cleaving enzyme 1 (BACE1) was determined by qRT-PCR and western blot. The binding ability between miR-340 and BACE1 was verified by dual-luciferase reporter assay. In vitro cell model of AD was established in human neuroblastoma SH-SY5Y cells transfected with Swedish mutant form of amyloid precursor protein (APPswe). The effect of miR-340 on the accumulation of amyloid- ß was investigated by western blot analysis. Flow cytometry was conducted to detect cell apoptosis. RESULTS: MiR-340 was down-regulated in the hippocampus of AD model SAMP8 mouse compared to SAMR1 mouse, while BACE1 was up-regulated in SAMP8, suggesting a negative correlation between miR-340 and BACE1 in SAMP8 mouse. MiR-340 could directly bind with BACE1, and over-expression of miR-340 decreased expression of BACE1 in SH-SY5Y/APPswe cells. MiR- 340 reduced the accumulation of amyloid-ß and suppressed cell apoptosis through targeting BACE1 in SH-SY5Y/APPswe cells. CONCLUSION: MiR-340 was downregulated in AD and reduced the accumulation of amyloid-ß through targeting BACE1, suggesting a potential therapeutic target for AD.