As the average age and life expectancy increases, the incidence of both acute and chronic central nervous system (CNS) pathologies will increase. Understanding mechanisms underlying neuroinflammation as the common feature of any neurodegenerative pathology, we can exploit the pharmacology of cell specific ion channels to improve the outcome of many CNS diseases. As the main cellular player of neuroinflammation, microglia play a central role in this process. Although microglia are considered non-excitable cells, they express a variety of ion channels under both physiological and pathological conditions that seem to be involved in a plethora of cellular processes. Here, we discuss the impact of modulating microglia voltage-gated, potential transient receptor, chloride and proton channels on microglial proliferation, migration, and phagocytosis in neurodegenerative diseases.

(1) Background: As membrane channels contribute to different cell functions, understanding the underlying mechanisms becomes extremely important. A large number of neuronal channels have been investigated, however, less studied are the channels expressed in the glia population, particularly in microglia. In the present study, we focused on the function of the Kv1.3, Kv1.5 and Kir2.1 potassium channels expressed in both BV2 cells and primary microglia cultures, which may impact the cellular migration process. (2) Methods: Using an immunocytochemical approach, we were able to show the presence of the investigated channels in BV2 microglial cells, record their currents using a patch clamp and their role in cell migration using the scratch assay. The migration of the primary microglial cells in culture was assessed using cell culture inserts. (3) Results: By blocking each potassium channel, we showed that Kv1.3 and Kir2.1 but not Kv1.5 are essential for BV2 cell migration. Further, primary microglial cultures were obtained from a line of transgenic CX3CR1-eGFP mice that express fluorescent labeled microglia. The mice were subjected to a spared nerve injury model of pain and we found that microglia motility in an 8 µm insert was reduced 2 days after spared nerve injury (SNI) compared with sham conditions. Additional investigations showed a further impact on cell motility by specifically blocking Kv1.3 and Kir2.1 but not Kv1.5; (4) Conclusions: Our study highlights the importance of the Kv1.3 and Kir2.1 but not Kv1.5 potassium channels on microglia migration both in BV2 and primary cell cultures.

Background: Myocardial infarction (MI) in young adults, once a rarity, is increasingly recognized as a distinct clinical entity. Unlike traditional MI patients, younger individuals often present without established risk factors or advanced atherosclerosis, prompting a reevaluation of pathophysiologic paradigms and risk assessment strategies. Objective: This review synthesizes current evidence on the epidemiology, pathophysiology, and diagnostic challenges of MI in adults under 55 years, with emphasis on risk factor profiles. We distinguish between traditional cardiovascular risk factors—smoking, dyslipidemia, hypertension, diabetes, obesity, and family history—and emerging contributors, including elevated lipoprotein(a), recreational drug use (cocaine, cannabis, amphetamines), autoimmune and inflammatory conditions, psychosocial stress, sleep disorders, genetic predisposition, and non-atherosclerotic mechanisms such as myocardical infarction with non-obstructive coronary arteries, spontaneous coronary artery dissection, SCAD and Takotsubo syndrome. Methods: A narrative literature review was conducted, focusing on studies from the last five years addressing MI in young adults, including data from large registries, cohort studies, and recent experimental findings.

Sepsis remains a major medical emergency that describes the body's systemic immune response to an infectious process and can lead to end-stage organ dysfunction and death. Clinical studies have introduced the concept of sepsis associated encephalopathy, which seems to have a plethora of cellular and molecular triggers starting from systemic inflammatory cytokines, blood-brain barrier (BBB) rupture, microscopic brain injury, altered cerebral circulation, neurotransmission, or even metabolic dysfunction. The purpose of our study is to reproduce the sepsis model previously described using the cecal ligature and puncture (CLP), and to take a closer look to the acute modifications that occur on cellular level when it comes to the brain-blood-barrier of the mice with systemic inflammation. After a rapid systemic response to peritonitis, we show a heterogeneity in astrocytic response within different cortical structures; hippocampus having the longest change in the number of GFAP+cells, while no difference was seen in the number of cortical astrocytes. With even more increasing roles of astrocytes in different pathologies, the relation between sepsis and astrocytes could prove a valuable in discovering new therapy in sepsis.

Background: The incidence of acute myocardial infarction (AMI) in young adults has been steadily rising, emphasizing the need for new biomarkers to improve risk stratification. Lipoprotein(a) (Lp(a)), a genetically determined lipoprotein with pro-atherogenic and pro-thrombotic properties, has gained increasing attention in this context. Methods: We evaluated serum Lp(a) levels in young patients with AMI and compared them with healthy controls. Associations between elevated Lp(a) levels (≥30 mg/dL) and coronary artery disease patterns were analyzed separately for STEMI and NSTEMI presentations. Results: Elevated Lp(a) levels were significantly more common in young patients with AMI compared with healthy controls. Importantly, Lp(a) ≥ 30 mg/dL was strongly associated with multivessel coronary artery disease in NSTEMI, conferring more than a fourfold increased risk. In STEMI, the effect was weaker and largely influenced by concomitant factors such as diabetes and elevated LDL cholesterol. Conclusions: These findings highlight key pathophysiological differences between infarct phenotypes and position Lp(a) as a particularly relevant biomarker in young NSTEMI patients. The systematic assessment of Lp(a) may enhance coronary risk stratification and support more tailored secondary prevention strategies.

Multiple sclerosis (MS) is a chronic progressive neurodegenerative disease that leads to disabilities such as difficulty moving and slowed cognitive processing. It is the leading non-traumatic cause of disability worldwide. MS also has a high potential to become a model for neurodegenerative diseases with a progression like Alzheimer’s or Parkinson’s. Cardiovascular diseases (CVDs) remain the leading cause of global deaths and have a considerable economic impact. The higher incidence of cardiovascular comorbidities in patients with MS compared to healthy individuals of the same age worsens the prognosis of neurological pathology, leading to a higher level of disability, poorer physical outcomes, higher depression scores, cognitive aging, and diminished quality of life. Classical observational studies often have questionable elements that can represent a source of error, making it difficult to establish a causal relationship between MS and CVD. Genetic studies, including genome-wide evaluation, may resolve this issue and may represent a topic for future research. We report the case of a 31-year-old male patient with a history of multiple sclerosis (MS) diagnosed seven years prior, who presented with acute chest pain upon returning from vacation. Despite the previous recommendation for disease-modifying therapy, the patient had discontinued treatment by personal choice. Electrocardiography (ECG) revealed ST-segment elevation in inferior leads, and emergent coronary angiography identified severe multi-vessel coronary artery disease (CAD), requiring immediate revascularization. This case highlights the potential cardiovascular risks in young patients with MS and the importance of continuous medical supervision.