Pseudomonas aeruginosa is a complex nosocomial infectious agent responsible for numerous illnesses, with its growing resistance variations complicating treatment development. Studies have emphasized the importance of virulence factors OprE and OprF in pathogenesis, highlighting their potential as vaccine candidates. In this study, B-cell, MHC-I, and MHC-II epitopes were identified, and molecular linkers were active to join these epitopes with an appropriate adjuvant to construct a vaccine. Computational tools were employed to forecast the tertiary framework, characteristics, and also to confirm the vaccine’s composition. The potency was weighed through population coverage analysis and immune simulation. This project aims to create a multi-epitope vaccine to reduce P. aeruginosa–related illness and mortality using immunoinformatics resources. The ultimate complex has been determined to be stable, soluble, antigenic, and non-allergenic upon inspection of its physicochemical and immunological properties. Additionally, the protein exhibited acidic and hydrophilic characteristics. The Ramachandran plot, ProSA-web, ERRAT, and Verify3D were employed to ensure the final model’s authenticity once the protein’s three-dimensional structure had been established and refined. The vaccine model showed a significant binding score and stability when interacting with MHC receptors. Population coverage analysis indicated a global coverage rate of 83.40%, with the USA having the highest coverage rate, exceeding 90%. Moreover, the vaccine sequence underwent codon optimization before being cloned into the Escherichia coli plasmid vector pET-28a (+) at the EcoRI and EcoRV restriction sites. Our research has developed a vaccine against P. aeruginosa that has strong binding affinity and worldwide coverage, offering an acceptable way to mitigate nosocomial infections.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder responsible for 50–75% of dementia cases worldwide, primarily affecting individuals over 65 years of age. It is characterized by cognitive decline, memory loss, and behavioral abnormalities. Key pathological features include extracellular β-amyloid (Aβ) plaques, intracellular neurofibrillary tangles of hyperphosphorylated tau protein, mitochondrial dysfunction, and cholinergic system impairment. Despite extensive research, the precise etiology remains unclear, and current treatments only alleviate symptoms without halting disease progression. A comprehensive literature review was conducted using peer-reviewed articles from PubMed, Scopus, and Google Scholar, emphasizing recent studies on molecular mechanisms, risk factors, diagnostics, and therapies. Major pathogenic mechanisms identified include oxidative stress, tau hyperphosphorylation, Aβ aggregation, and synaptic degeneration. Non-modifiable risk factors such as aging, genetic mutations in amyloid precursor protein, phosphatidylinositol-binding clathrinid assembly protein, presenilin 1/2, and the apolipoprotein E ε4 allele play significant roles, whereas modifiable risks involve lifestyle factors and comorbidities such as diabetes. Diagnostic advancements highlight the promise of blood-based biomarkers, although current practices rely heavily on cerebrospinal fluid markers and neuroimaging. Approved pharmacological interventions, including cholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists, provide limited symptomatic relief. Ongoing research into Aβ- and tau-targeted therapies has yielded mixed results. In addition, novel approaches such as tripartite motif-containing protein 2-mediated tau clearance and deep cervical lymphatic-venous anastomosis are being explored for their potential in targeting intracellular aggregates and enhancing brain waste clearance. AD emerges as a multifactorial condition driven by a complex interplay of biological, genetic, and environmental factors. Although substantial progress has been made in understanding its pathophysiology, effective disease-modifying therapies remain elusive. Continued advances in biomarker discovery and personalized therapeutic strategies offer hope for improved early detection and targeted treatment approaches.