Neurodegenerative diseases are characterized by neuroinflammation, neuronal depletion and oxidative stress. They coincide with subtle chronic or flaring inflammation, sometimes escalating with infiltrations of the immune system cells in the inflamed parts causing mild to severe or even lethal damage. Thus, neurodegenerative diseases show all features of autoimmune diseases. Prevalence of neurodegenerative diseases has dramatically increased in recent decades and unfortunately, the therapeutic efficacy and safety profile of available drugs is moderate. The beneficial effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) polyunsaturated fatty acids (omega-3 PUFAs) are nowadays highlighted by a plethora of studies. They play a role in suppression of inflammation, gene expression, cellular membrane fluidity/permeability, immune functionality and intracellular/exocellular signaling. The role of omega-6 polyunsaturated fatty acids, such as linoleic acid (LA), gamma linolenic acid (GLA), and arachidonic acid (AA), on neuroprotection is controversial, as some of these agents, specifically AA, are proinflammatory, whilst current data suggest that they may have neuroprotective properties as well. This review provides an overview of the existing recent clinical studies with respect to the role of omega-3 and omega-6 PUFAs as therapeutic agents in chronic, inflammatory, autoimmune neurodegenerative diseases as well as the dosages and the period used for testing.

Cardiovascular disease (CVD) that includes myocardial infarction and stroke, is the leading cause of mortality worldwide. Atherosclerosis, the primary underlying cause of CVD, can be controlled by pharmacological and dietary interventions, including n-3 polyunsaturated fatty acid (PUFA) supplementation. n-3 PUFA supplementation, primarily consisting of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), has shown promise in reducing atherosclerosis by modulating risk factors, including triglyceride levels and vascular inflammation. n-3 PUFAs act by replacing pro-inflammatory fatty acid types in cell membranes and plasma lipids, by regulating transcription factor activity, and by inducing epigenetic changes. EPA and DHA regulate cellular function through shared and differential molecular mechanisms. Large clinical studies on n-3 PUFAs have reported conflicting findings, causing confusion among the public and health professionals. In this review, we discuss important factors leading to these inconsistencies, in the context of atherosclerosis, including clinical study design and the differential effects of EPA and DHA on cell function. We propose steps to improve clinical and basic experimental study design in order to improve supplement composition optimization. Finally, we propose that understanding the factors underlying the poor response to n-3 PUFAs, and the development of molecular biomarkers for predicting response may help towards a more personalized treatment.

In the healthcare sector, phytocompounds are known to be beneficial by contributing or alleviating a variety of diseases. Studies have demonstrated the progressive effects of phytocompounds on immune-related diseases and to exhibit anticancer effects. Graviola tree is an evergreen tree with its extracts (leafs and seeds) been reported having anticancer properties, but the precise target of action is not clear. Using an in silico approach, we predicted that annonacin, an Acetogenin, the active agent found in Graviola leaf extract (GLE) to potentially act as a novel inhibitor of both sodium/potassium (NKA) and sarcoplasmic reticulum (SERCA) ATPase pumps. We were able to validate and confirm the in silico studies by showing that GLE inhibited NKA and SERCA activity in intact cells. In the present study, we also demonstrated the antiproliferative and anticancer effects of GLE in a variety of cancer cell lines with limited toxic effects on non-transformed cells. Moreover, our results revealed that known inhibitors of both NKA and SERCA pumps could also promote cell death in several cancer cell lines. In addition, a mouse xenograft cancer model showed GLE as able to reduce tumor size and progression. Finally, bioprofiling studies indicated a strong correlation between overexpression of both NKA and SERCA gene expression vs. survival rates. Overall, our results demonstrated that GLE can promote selective cancer cell death via inhibiting NKA and SERCA, and thus can be considered as a potential novel treatment for cancer. After molecular analysis of GLE by liquid chromatography–mass spectrometry and ESI–QTOF–MS analysis, it was found that the MS spectrum of the high abundant chromatographic peak purified sample highly consisted of annonacin.

Transthyretin amyloidosis (ATTR) is a progressive systemic disorder driven by the misfolding of transthyretin (TTR) proteins and their deposition as amyloid fibrils. It manifests as hereditary ATTR (ATTRv), caused by pathogenic variants, and wild-type ATTR (ATTRwt), linked primarily to aging. These deposits preferentially affect the myocardium and peripheral nerves, producing severe cardiomyopathy and polyneuropathy. The amyloidogenic cascade is initiated by the dissociation of TTR tetramers into misfolded monomers that aggregate into insoluble fibrils. Historically, treatment was limited to supportive care or organ transplantation; however, it has been transformed by TTR stabilizers, RNA interference (RNAi) agents, and antisense oligonucleotides (ASOs). More recently, CRISPR-Cas9 genome editing has emerged as a potential single-dose strategy for durable TTR suppression. In parallel, anti-fibril therapies, including amyloid-depleting monoclonal antibodies designed to clear existing tissue deposits, are being developed as a complementary disease-modifying strategy. This review delineates the molecular mechanisms of amyloidogenesis and evaluates current clinical management strategies. Recent advances in noninvasive diagnostics and targeted molecular therapies, enabled by precision medicine, have markedly improved disease management and clinical outcomes.

The 10th International Multithematic Bio-Medical Congress (IMBMC) 2022, "Bio-Medical Scientific Cyprus," took place at European University Cyprus (EUC), Nicosia, Cyprus, under the auspices of the Ministry of Health and the Cyprus Medical Association. IMBMC is an internationally recognized event that was founded and established by Professor Dr Ioannis Patrikios, the Deputy Dean and Faculty member of the School of Medicine at EUC. During the 10th IMBMC, both Sir Gregory Winter (Nobel Prize in Chemistry, 2018, on protein and antibody engineering and antibody therapies) and Sir Martin Evans (awarded the 2007 Nobel Prize in Physiology or Medicine for his groundbreaking discoveries on embryonic stem cells and DNA recombination in mammals) were announced as Honorary Professors of the School of Medicine, European University Cyprus. The first honorary keynote speaker Professor Sir Gregory Winter's contribution engaged in the science of protein engineering. Being the founder of both Cambridge Antibody Technology (1989) and Domantis (2000), he spearheaded the use of a new class of drugs using engineered antibody technology to treat pathological diseases. At the Laboratory of Molecular Biology, Dr Winter focused on innovating techniques to familiarize the use of antibodies in the field of therapeutics, with his goal being to develop entirely humanized antibodies, using combinational gene repertoires. Over half of the antibodies sold today are a result of his inventions, including the humanized antibodies Campath-1H, Herceptin, Avastin, Synagis, and the first human antibody (Humira) to receive approval by the US Food and Drug Administration. Precisely, antibodies, as today's principal biological drug, especially for the treatment of cancer and autoimmune diseases, have replaced areas that were poorly served by chemical drugs. Will such developments thrive. Professor Dr Kypros Herodotou Nicolaides spoke on preeclampsia (PE), which is a leading cause of maternal mortality and severe morbidity, in association with increased perinatal risks. He focused on ways to approach PE. These included actions on specific weeks and interventions to tackle PE, the rate, and the rate of term. Three methods were used. The first method to target PE was aspirin (150 mg per day from 12 to 36 weeks reduced the rate of PE <32 weeks by 90%, PE <37 weeks by 60%), which had no effect on term PE. The second one included the incorporation of maternal characteristics in blood pressure, serum placental growth factor, and serum sFlt-1, which identified about 70% of women who