👤 Mansoureh Eslami

Elevated levels of lipoprotein(a) [Lp(a)] are increasingly recognized as an independent risk factor for cardiovascular diseases (CVDs). This systematic review and meta-analysis aimed to evaluate the impact of lipid apheresis therapy on serum Lp(a) levels in a wide array of disorders, particularly CVDs. Following PRISMA guidelines, we searched PubMed, Scopus, and Web of Science databases up to May 2025. Studies reporting pre- and post-treatment Lp(a) levels in participants undergoing lipid apheresis were included. A random-effects model was used when heterogeneity was significant. Subgroup and meta-regression analyses were conducted to explore potential sources of heterogeneity. A total of 43 publications comprising 67 studies with 2466 participants were analysed. Lipid apheresis significantly reduced serum Lp(a) levels (SMD = -1.52; 95% CI = -1.76 to -1.29; P < 0.001). Subgroup analyses confirmed significant reductions across various methods of Lp(a) detection, disease backgrounds, and initial Lp(a) levels. One-session lipid apheresis studies (n = 6) also demonstrated a significant reduction (SMD = -1.51; 95% CI = -1.72 to -1.29; P < 0.001). Meta-regression suggested that publication year and disease background contributed to heterogeneity. Lipid apheresis is effective in significantly lowering serum Lp(a) concentrations across a range of patient groups and treatment modalities. These findings support the therapeutic role of lipid apheresis in managing elevated Lp(a). Show less

Chronic cerebral hypoperfusion (CCH), a pathophysiological state linked to vascular dementia and cognitive impairment, involves the NgR1/Lingo-1/p75 signaling complex implicated in neurodegenerative processes. Resveratrol (RES), a neuroprotective compound, was investigated for its potential to mitigate CCH-induced cognitive deficits by targeting this pathway. This study examined RES's ability to improve cognitive impairment in CCH by suppressing the NgR1/Lingo-1/p75 complex and downstream RhoA-ROCK2 signaling. Rats were divided into five groups: Control, CCH + Ethanol (ETH), CCH, CCH + resveratrol (RES), and RES. Chronic cerebral hypoperfusion was induced via permanent bilateral carotid artery occlusion (2VO). Cognitive function was assessed using the Morris Water Maze (MWM). Hippocampal morphology in CA1, CA3, and dentate gyrus (DG) regions was analyzed via H&E staining. The expression levels of Lingo-1, NgR1, P75, RhoA, and ROCK2 signaling pathway were detected by western blot and quantitative real-time PCR (qRT-PCR). Chronic cerebral hypoperfusion rats showed elevated protein expression of Lingo-1, p75, RhoA, and ROCK2, though NgR1 remained unchanged. The RES treatment significantly reduced these protein levels. Similarly, mRNA levels of all five targets increased in CCH, but RES notably lowered Lingo-1 and NgR1 expression. The MWM tests revealed RES improved spatial learning and memory deficits in 2VO rats. H&E staining demonstrated RES's neuroprotective effects, preserving hippocampal neuron integrity. Resveratrol alleviates CCH-induced cognitive impairment by downregulating the Lingo-1/NgR1/p75 signaling axis and inhibiting RhoA-ROCK2 pathways. These findings highlight RES's potential as a therapeutic agent for vascular cognitive impairment associated with chronic hypoperfusion. Show less

Multiple sclerosis (MS) is an autoimmune central nervous system (CNS) disorder indicated by demyelination, chronic inflammation, and neuronal destruction. Regional demyelination, inflammation responses, scar development, and various axonal damage are pathological characteristics of MS. Curcumin is a hydrophobic polyphenol extracted from the rhizome of the turmeric plant. In addition to anti-inflammatory effects, beneficial therapeutic effects such as antioxidant, anti-cancer and nerve protection have also been seen from this compound. The purpose of the current investigation was to provide light on the potential benefits of Curcumin in treating experimental autoimmune encephalomyelitis (EAE), the animal model of MS. in Female C57BL/6 mice were used to induce EAE through myelin oligodendroglial glycoprotein (MOG). Curcumin doses of 100 and 200 mg/kg were administered orally in the treatment groups starting on the first day of EAE induction. Brains and splenocytes were extracted from euthanized animals on day 25 following EAE induction. Demyelination and leukocyte infiltration, proliferation, cytokine, and gene expression profiles were assessed. Our findings demonstrate that both low and high doses of Curcumin decreased the progression of EAE. Histological analyses revealed low infiltration of leukocytes into the CNS. Curcumin therapy enhanced Th2 and Treg cell secretion of IL-4, IL-10, and TGF-β although considerably decreasing IFN-γ and TNF-α. Curcumin-induced Th2 and Treg cell cytokine production and transcription factor gene expression (IL-13, GATA3, STAT6 and IL-35, CTLA4, Foxp3) and anti-inflammatory cytokines (IL-27, IL-33). Overall, these findings provide additional evidence that Curcumin can slow disease development and alleviate symptoms in EAE through stimulating Treg and Th2 cell polarization. They support Curcumin's potential therapeutic role in MS. Show less

Anhedonia or inability to experience pleasure is the sign of various neuropsychiatric conditions. Current treatment options do not provide adequate control of anhedonia. The present study was conducted to evaluate the protective effects of valproic acid (VPA) as a nonspecific histone deacetylase (HDAC) inhibitor to reverse the effects of stress on induction of anhedonia and explore possible mechanisms. To induce anhedonia, a rat model of chronic unpredictable mild stress (CUMS) was established. Animals were assigned into no stress, stress (6 weeks of CUMS) and two treatment groups. VPA treatment was carried out for 4 continuous weeks (200 mg/kg/day). Behavioral assessments were performed using sucrose consumption (SCT) and new object recognition (NOR) tests. The expression of genes was evaluated using qRT-PCR. The cell density was determined using Nissl staining. Rats with CUMS showed depressive-like behaviors and impaired memory performance compared with the non-stressed group (p < 0.01). Moreover, they had significantly higher levels of HDAC3 and MC4R expression in the nucleus accumbens (NAc) compared to the non-stressed group (p < 0.01). The NAc cell density was significantly higher in the non-stressed rats (p < 0.05). Corticosterone plasma level was increased in the CUMS compared to the non-stressed group (p < 0.05). In the CUMS + VPA subgroup, the corticosterone (CORT) plasma level was lower compared with the CUMS + Saline and/or the CUMS groups (p < 0.05). These findings suggest that VPA can improve anhedonia and stress. Although the protective effect of VPA might link to decreasing HDAC3 and MC4R genes expression in NAc. Show less

Peanut allergy (PA) is a complex disease with both environmental and genetic risk factors. Previously, PA loci were identified in filaggrin (FLG) and HLA in candidate gene studies, and loci in HLA were identified in a genome-wide association study and meta-analysis. We sought to investigate genetic susceptibility to PA. Eight hundred fifty cases and 926 hyper-control subjects and more than 7.8 million genotyped and imputed single nucleotide polymorphisms (SNPs) were analyzed in a genome-wide association study to identify susceptibility variants for PA in the Canadian population. A meta-analysis of 2 phenotypes (PA and food allergy) was conducted by using 7 studies from the Canadian, American (n = 2), Australian, German, and Dutch (n = 2) populations. An SNP near integrin α6 (ITGA6) reached genome-wide significance with PA (P = 1.80 × 10 This study identifies multiple novel loci as risk factors for PA and food allergy and establishes C11orf30 as a risk locus for both PA and food allergy. Multiple genes (C11orf30/EMSY, SKAP1, and CTNNA3) identified by this study are involved in epigenetic regulation of gene expression. Show less