The brain-derived neurotrophic factor (BDNF) has become one of the cornerstones of neuropathology, influencing synaptic plasticity, cognitive resilience, and neuronal survival. Apart from its molecular biology, BDNF is a powerful target for transformative benefit in precision medicine, leading to innovative therapeutic approaches for neurodegenerative and psychiatric diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD), major depressive disorder (MDD), and post-traumatic stress disorder (PTSD). Nevertheless, clinical applicability is obstructed by hurdles in delivery, patient-specific diversity, and pleiotropic signaling. Here, we summarize findings in BDNF research, including its regulatory pathways and diagnostic/prognostic biomarkers and integrative therapeutic approaches. We describe innovative delivery systems, such as lipid nanoparticle-based mRNA therapies and CRISPR-dCas9-based epigenetic editing that bypass obstacles such as BBB (blood–brain barrier) and enzymatic degradation. The recent implementation of multiplex panels combining BDNF biodynamic indicators with tau and amyloid-β signaling markers showcases novel levels of specificity for both early detection and potential therapeutic monitoring. Humanized preclinical models like iPSC-derived neurons and organoids point to the key role of BDNF in neurodeveloping and neurodegenerative processes, paralleling advances in bridging preclinical observation and clinical environments. Moreover, novel therapeutic tools delivering TrkB activators or the implementation of AI-based dynamic care platforms enable tailored and scalable treatments. This review also aims to extend a framework used in the understanding of BDNF’s relevance to traditional neurodegenerative models by situating more recent work detailing BDNF’s actions in ischemic tissues and the gut–brain axis in the context of systemic health. Finally, we outline a roadmap for the incorporation of BDNF-centered therapies into worldwide healthcare, highlighting ethical issues, equity, and interdisciplinary decomposition. The therapeutic potential of BDNF heralds a new era in neuroscience and medicine, revolutionizing brain health and paving the way for the advancement of precision medicine.

Neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, ALS, and Huntington’s, remain formidable challenges in medicine, with their relentless progression and limited therapeutic options. These diseases arise from a web of molecular disturbances—misfolded proteins, chronic neuroinflammation, mitochondrial dysfunction, and genetic mutations—that slowly dismantle neuronal integrity. Yet, recent scientific breakthroughs are opening new paths to intervene in these once-intractable conditions. This review synthesizes the latest insights into the underlying molecular dynamics of neurodegeneration, revealing how intertwined pathways drive the course of these diseases. With an eye on the most promising advances, we explore innovative therapies emerging from cutting-edge research: nanotechnology-based drug delivery systems capable of navigating the blood–brain barrier, gene-editing tools like CRISPR designed to correct harmful genetic variants, and stem cell strategies that not only replace lost neurons but foster neuroprotective environments. Pharmacogenomics is reshaping treatment personalization, enabling tailored therapies that align with individual genetic profiles, while molecular diagnostics and biomarkers are ushering in an era of early, precise disease detection. Furthermore, novel perspectives on the gut–brain axis are sparking interest as mounting evidence suggests that microbiome modulation may play a role in reducing neuroinflammatory responses linked to neurodegenerative progression. Taken together, these advances signal a shift toward a comprehensive, personalized approach that could transform neurodegenerative care. By integrating molecular insights and innovative therapeutic techniques, this review offers a forward-looking perspective on a future where treatments aim not just to manage symptoms but to fundamentally alter disease progression, presenting renewed hope for improved patient outcomes.

Neuroimmunology is reshaping the understanding of the central nervous system (CNS), revealing it as an active immune organ rather than an isolated structure. This review delves into the unprecedented discoveries transforming the field, including the emerging roles of microglia, astrocytes, and the blood–brain barrier (BBB) in orchestrating neuroimmune dynamics. Highlighting their dual roles in both repair and disease progression, we uncover how these elements contribute to the intricate pathophysiology of neurodegenerative diseases, cerebrovascular conditions, and CNS tumors. Novel insights into microglial priming, astrocytic cytokine networks, and meningeal lymphatics challenge the conventional paradigms of immune privilege, offering fresh perspectives on disease mechanisms. This work introduces groundbreaking therapeutic innovations, from precision immunotherapies to the controlled modulation of the BBB using nanotechnology and focused ultrasound. Moreover, we explore the fusion of immune modulation with neuromodulatory technologies, underscoring new frontiers for personalized medicine in previously intractable diseases. By synthesizing these advancements, we propose a transformative framework that integrates cutting-edge research with clinical translation, charting a bold path toward redefining CNS disease management in the era of precision neuroimmunology.

Background: First described by Carl Toldt in the late 19th century, the mesorectum has since been a topic of anatomical and surgical debate. Its clinical importance was redefined by Heald’s introduction of Total Mesorectal Excision (TME), nowadays the golden standard in oncologic rectal surgery. This study aims to elucidate the embryological development and adult anatomy of the mesorectum and the mesorectal fascia, with a focus on clinically significant relations, particularly the peritoneum, and components of the hypogastric plexuses. Methods: We performed anatomical dissections on four 12–15-week-old human fetuses and eight formalin-fixed adult cadavers. In addition, a transverse pelvic section was examined to assess the spatial organization of mesorectal and fascial structures. Results: Our findings confirm the presence of a dorsal mesentery at the rectal level during fetal development, illustrating its transformation into the adult mesorectum. We identified the mesorectal contents in the fetus and examined the course and relations of the superior rectal vessels, hypogastric nerves, and pelvic splanchnic nerves, in both fetal and adult specimens. Conclusions: The observed fetal and adult configurations provide a continuous morphological description of the mesorectum and its compartmental organization within the pelvis. This study enhances the understanding of the mesorectum’s embryology, structure, and vital surgical landmarks. By delineating the so-called ‘Holy plane’ of Heald (the natural avascular plane between the mesorectal and presacral fasciae used during total mesorectal excision) and the delicate connective fibers known surgically as ‘angel’s hair’, which become visible when this plane is correctly entered, rectal and presacral fasciae, and neurovascular elements, provides a comprehensive anatomical framework that may inform surgical plane identification and support future clinical investigations into nerve-sparing rectal surgery.

Background: The concept of mesopancreas is frequently discussed in the surgical literature as the neural pathway for metastatic spread in pancreatic head cancer. It generally refers to a retro-pancreatic plane that should be resected to reduce the incidence of regional metastases. However, this concept remains poorly defined, both embryologically and anatomically. Our objective was to establish a clear embryological and anatomical definition of the mesopancreas, making anatomical data more applicable in surgical practice. Methods: We examined seven cadavers (5 males, 2 females, aged 62–71) with no medical or surgical history, preserved in 9% formalin at Carol Davila University’s Anatomy Department. Regional dissections were performed in successive planes, highlighting the celiac ganglia and the associated network of neural connections that comprise the mesopancreas. Results: Our study defines the “mesopancreas” as remnants of primordial mesenteries that coalesced into the Treitz fascia. We identified its functional components as nerve fibers linking the celiac ganglia and superior mesenteric plexus to the pancreas, along with vascular structures, lymphatics, and connective and adipose tissue. These components likely contribute to regional metastasis in pancreatic head cancer. While resection of the mesopancreas could help prevent metastasis, its complex anatomy and proximity to major vessels pose significant surgical challenges. Conclusions: Based on our findings, we propose a plausible definition for the term “mesopancreas”. It encompasses the structures that originated as part of the primordial mesenteries, which subsequently coalesced, resulting in the formation of the Treitz fascia. In essence, the mesopancreas is the functional content of a former mesentery.

We report a case of a 63-year-old male patient with multiple cardiovascular risk factors and previous myocardial infarction who was referred to the emergency department on September 2023 with symptoms and clinical and biological data consistent with an acute coronary event. A coronary angiography revealed severe ostial stenosis of the left anterior descending artery (LAD) and intrastent thrombotic occlusion in the first two segments of the LAD. Two drug-eluting stents were implanted and the patient was discharged when hemodynamically stable; however, three weeks later, he returned to the emergency department complaining of fever, anterior chest pain, dyspnea at rest, and high blood pressure values at home. High levels of troponin T, C-reactive protein, and NT-proBNP were detected and blood cultures showed methicillin-resistant Staphylococcus aureus. The computed tomography (CT) examination showed a saccular dilatation had developed between two fragments of a stent mounted at the level of the LAD, surrounded by a hematic pericardial accumulation. LAD pseudoaneurysm ablation and a double aortocoronary bypass with inverted saphenous vein autograft were performed and the patient showed a favorable postoperative evolution. In this case, surgical revascularization was proven to be the appropriate treatment strategy, demonstrating the need to choose an individualized therapeutic option depending on case-specific factors.