👤 Hossein Poustchi

The present study aims to investigate the impact of stroke history on cognitive function, white matter hyperintensities (WMHs), and circulating brain-derived neurotrophic factor (BDNF) levels in brain lesion patients. In this study, we enrolled 228 individuals exhibiting clinical symptoms of stroke from the Golestan Cohort Study. The participants were categorized into two groups based on their stroke history. Subsequently, 120 patients with a history of stroke and 108 patients without obvious brain lesions were subjected to comparative analysis using magnetic resonance imaging (MRI). Montreal Cognitive Assessment (MoCA) and Fazekas scores were used to evaluate cognitive function and WMH burden, respectively. In addition, circulating BDNF levels were measured using the Human BDNF Elisa kit. Totally, 228 patients were recruited in the study with a mean age of 63.8 years. Stroke was found in 52.6%. MoCA scores and plasma BDNF levels were significantly lower in patients with a history of stroke compared to people without such a history after adjusting for age, sex, education and type of residency (adjusted regression coefficient (RC) (95% CI)=-4.0 (-5.0 to -3.0), -3.2 (-4.2 to -2.2), respectively). In addition, the intensity burden of white matter was higher in the stroke group (adjusted RC (95% CI)=1.2 (0.8 to 1.6). The study suggests that a multi-biomarker approach, encompassing measures such as the MoCA score, Fazekas score, and circulating BDNF levels, can provide valuable insight into the neurological status of post-stroke patients and highlight potential avenues for improving patient outcomes through early detection and intervention strategies. Show less

Recent evidence has demonstrated a strong interplay and multifaceted relationship between non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). CVD is the major cause of death in patients with NAFLD. NAFLD also has strong associations with diabetes and metabolic syndrome. In this comprehensive review, we aimed to overview the primary environmental and genetic risk factors of NAFLD, and CVD and also focus on the genetic aspects of these two disorders. NAFLD and CVD are both heterogeneous diseases with common genetic and molecular pathways. We have searched for the latest published articles regarding this matter and tried to provide an overview of recent insights into the genetic aspects of NAFLD and CVD. The common genetic and molecular pathways involved in NAFLD and CVD are insulin resistance (IR), subclinical inflammation, oxidative stress, and atherogenic dyslipidemia. According to an investigation, the exact associations between genomic characteristics of NAFLD and CVD and casual relationships are not fully determined. Different gene polymorphisms have been identified as the genetic components of the NAFLDCVD association. Some of the most documented ones of these gene polymorphisms are patatin-like phospholipase domain-containing protein 3 (PNPLA3), transmembrane 6 superfamily member 2 (TM6SF2), hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13), adiponectin-encoding gene (ADIPOQ), apolipoprotein C3 (APOC3), peroxisome proliferator-activated receptors (PPAR), leptin receptor (LEPR), sterol regulatory element-binding proteins (SREBP), tumor necrosis factor-alpha (TNF-α), microsomal triglyceride transfer protein (MTTP), manganese superoxide dismutase (MnSOD), membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), and mutation in DYRK1B that substitutes cysteine for arginine at position 102 in kinase-like domain. Further cohort studies with a significant sample size using advanced genomic assessments and next-generation sequencing techniques are needed to shed more light on genetic associations between NAFLD and CVD. Show less

Non-alcoholic fatty liver disease (NAFLD) is associated with a substantial increased risk of atherosclerotic cardiovascular disease (ASCVD), which is partly related to dyslipidemia and low HDL-C level. The cardioprotective activity of HDL in the body is closely connected to its role in promoting cholesterol efflux, which is determined by cholesterol efflux capacity (CEC). Hitherto, the role of HDL, as defined by CEC has not been assessed in NAFLD patients. In this research study, we present the results of a study of cAMP-treated J774 CEC and THP-1 macrophage CEC in ApoB-depleted plasma of 55 newly diagnosed NAFLD patients and 30 controls. Circulating levels of ApoA-I, ApoB, preβ-HDL, plasma activity of CETP, PLTP, LCAT and carotid intima-media thickness (cIMT) were estimated. cAMP-treated J774 and THP-1 macrophage CEC were found to be significantly lower in NAFLD patients compared to controls (P < 0.001 and P = 0.003, respectively). In addition, it was discovered that both ApoA-I and preβ1-HDL were significantly lower in NAFLD patients (P < 0.001). Furthermore, cAMP-treated J774 CEC showed independent negative correlation with cIMT, as well as the presence of atherosclerotic plaque in NAFLD patients. In conclusion, our findings showed that HDL CEC was suppressed in NAFLD patients, and impaired cAMP-treated J774 CEC was an independent risk factor for subclinical atherosclerosis in NAFLD patients, suggesting that impaired HDL functions as an independent risk factor for atherosclerosis in NAFLD. Show less