Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, yet its underlying causes remain elusive. The conventional perspective on disease pathogenesis attributes alterations in neuronal excitability to molecular changes resulting in synaptic dysfunction. Early hyperexcitability is succeeded by a progressive cessation of electrical activity in neurons, with amyloid beta (Aβ) oligomers and tau protein hyperphosphorylation identified as the initial events leading to hyperactivity. In addition to these key proteins, voltage-gated sodium and potassium channels play a decisive role in the altered electrical properties of neurons in AD. Impaired synaptic function and reduced neuronal plasticity contribute to a vicious cycle, resulting in a reduction in the number of synapses and synaptic proteins, impacting their transportation inside the neuron. An understanding of these neurophysiological alterations, combined with abnormalities in the morphology of brain cells, emerges as a crucial avenue for new treatment investigations. This review aims to delve into the detailed exploration of electrical neuronal alterations observed in different AD models affecting single neurons and neuronal networks.

Background: Small for gestational age neonates represent a population at risk of growth failure or deviant growth patterns and long-term metabolic complications. Breastfeeding has been identified as a critical factor in promoting healthier growth and long-term metabolic health in both full-term and preterm appropriate for gestational age infants, but similar studies in small for gestational age infants are limited. The aim of this narrative review is to assess the impact of breastfeeding on growth and body composition in small for gestational age neonates. Methods: The PubMed and Google Scholar databases were screened for the relevant literature. The following terms, were used: “low birth weight”, “in utero growth restriction”, “small for gestational age”, “human milk”, and “growth”. The initial screening identified 57 relevant studies. Thirteen of them fulfilled the eligibility criteria and were included in this narrative review. Results: In preterm small for gestational age neonates, human milk nutrition was associated with healthier catch-up growth without excessive fat accumulation. Fortification strategies were associated with enhanced growth outcomes without increased incidence of neonatal morbidities. In the context of full-term, small for gestational age neonates, exclusive breastfeeding has been demonstrated to be associated with healthy catch-up growth. Furthermore, human milk nutrition has been shown to mitigate the predisposition of these children to obesity and cardiometabolic complications. Conclusions: According to the limited extant literature, human milk feeding has been identified as a potentially protective factor for small for gestational age neonates, promoting healthier growth patterns and long-term cardiometabolic health. However, larger prospective studies are needed to evaluate human milk feeding and human milk fortification in association with growth and long-term outcomes in small for gestational age infants.

Valvular heart disease (VHD) represents a significant global health challenge, affecting over 2.5% of the population and disproportionately impacting older adults due to age‐related degenerative processes. Current treatment options—mechanical and bioprosthetic valves—both present substantial limitations that impact patient quality of life and long‐term outcomes. Mechanical valves require lifelong anticoagulation with associated bleeding risks, while bioprosthetic valves suffer from limited durability, typically requiring replacement within 10–15 years. These limitations are particularly problematic for pediatric and young adult populations, who face multiple surgical interventions throughout their lifetime. Decellularized scaffolds have emerged as promising alternatives due to their natural extracellular matrix architecture and potential for recipient cell repopulation and growth, making them especially valuable for pediatric patients. However, these scaffolds face several critical biological challenges that have prevented widespread clinical adoption, including suboptimal recellularization patterns, inflammatory responses, calcification propensity, and structural degradation over time. Recent advances in gene editing technologies, particularly CRISPR‐Cas9 and emerging base editing techniques, offer unprecedented opportunities to overcome these limitations by enabling precise molecular‐level tissue modifications. These technologies could enhance scaffold biocompatibility, promote favorable cellular responses, prevent calcification, and improve structural integrity. This review explores how combining decellularized scaffold approaches with gene editing techniques could transform heart valve treatment. We examine the potential of this integrated approach to create valve replacements with improved durability and biocompatibility and propose pathways for translating these innovations into clinical practice. The convergence of these technologies holds particular promise for younger patients who would benefit most from heart valves capable of growth and long‐term function without repeated surgical interventions.

The role of oxidative stress in chronic pathological conditions of the nervous system is well-established, contributing to neuronal dysfunction and cell death. Numerous studies have sought pharmacologic agents with antioxidant effects for neurons, with controversial results. Our study aims to establish a valid and reproducible in vitro oxidative stress model in neurons, simulating initial stages of neurodegenerative disorders, focusing on morphological alterations in the dendritic field of neurons. Primary hippocampal cells from newborn rat brains were cultured for two weeks, and subsequently, different concentrations of hydrogen peroxide (H₂O₂) were applied for 24 h in cultures. Cell viability assays and flow cytometry were carried out to measure H₂O₂ effects on apoptosis, necrosis, and reactive oxygen species production. Finally, morphometric evaluation of the neuronal dendritic field was conducted, focused on dendritic length, branching, and spine density, with ImageJ software following immunostaining of neurons. Administration of 100 μΜ H₂O₂ for 24 h in primary hippocampal cultures resulted in significant alterations in dendritic morphology (one-way ANOVA, p < 0.05), without significantly affecting cell viability. These results demonstrate the impact of H₂O₂ on neuronal morphology and suggest that dendritic and spinal alterations could serve as sensitive markers of mild oxidative stress on neurons, prior to the activation of apoptotic mechanisms. This can be used as a surrogate model for the initial stages of neurodegenerative disorders when synaptic loss takes place, facilitating study of agent effectiveness with antioxidant therapeutic potential.

NHE‐1 is a Na ⁺ /H ⁺ exchanger that receives phosphorylation signals, binds calmodulin and responds to neurohormonal input from angiotensin II, endothelin‐1, and adrenergic pathways. In cardiac myocytes, NHE‐1 maintains pH homeostasis and couples to Na ⁺ /Ca ²⁺ exchange and mitochondrial ion handling. During heart disease sustained activation drives intracellular Na ⁺ accumulation, promoting Ca ²⁺ overload and mitochondrial dysfunction. Oxidative stress then creates amplifying cycles that activate signaling pathways resulting to arrhythmias and fibrosis. Clinical trials failed despite preclinical promise, due to a variety of false experimental factors. SGLT2 inhibitors appear to modulate NHE‐1 indirectly through metabolic reprogramming and hemodynamic effects rather than direct blockade. Current approaches use structural data to target regulatory sites and phosphorylation‐dependent conformational states instead of the transport pore. Translation to patients will require biomarkers identifying pathological hyperactivity and better patient stratification methods. Here, we try to review NHE‐1 structure, regulation, and physiology that may influence research on future drug development.