Background: Prion diseases represent a group of rare, progressive, and invariably fatal neurodegenerative disorders. Their hallmark is the infectious nature of the misfolded prion protein (PrP^Sc), which propagates by inducing conformational changes in the physiological form (PrP^C). Despite advances in basic science, these disorders still pose major clinical and therapeutic challenges. Methods: A narrative review of the scientific literature was conducted across major biomedical databases, including PubMed, Scopus, Web of Science, and Google Scholar, covering publications up to January 2025. In addition, we describe an illustrative clinical case of a young patient with probable iatrogenic Creutzfeldt-Jakob disease following corneal transplantation, used to highlight diagnostic uncertainty and infection-control implications. Findings: Evidence confirms that PrP^Sc drives neurodegenerative processes and transmissibility, with phenotypic and genetic variants influencing clinical course and prognosis. From a diagnostic perspective, neuroimaging techniques and cerebrospinal fluid biomarkers have undergone substantial refinement, with RT-QuIC emerging as a highly specific and sensitive assay. Therapeutic options remain unsatisfactory: no treatment has shown a significant impact on survival. However, innovative strategies (including monoclonal antibodies, gene-based interventions, and modulation of PrP^C) represent promising avenues of investigation. Conclusions: Prion diseases remain an unresolved challenge at the intersection of neurology and infectious diseases. Earlier diagnosis through advanced biomarkers and continued development of targeted therapies are essential to improve patient management, while the persistence of iatrogenic cases underscores the ongoing relevance of surveillance and preventive strategies in clinical practice.

Alzheimer's disease (AD) is characterised by progressive neurodegeneration with the formation of amyloid beta (Aβ) plaques and neurofibrillary tau tangles in the brain parenchyma. The causes of AD have been attributed to a combination of age-related changes within the brain as well as genetic, environmental and lifestyle factors. However, a recent study by Banerjee et al. highlights the possibility that AD may be a transmissible disease and that iatrogenic AD could be environmentally acquired, similar to iatrogenic Creutzfeldt-Jakob disease (iCJD). The study reports that contaminated Aβ in cadaver-derived pituitary growth hormone (c-hGH) therapy, which patients received during childhood inoculation, may accidentally transmit into their brains, triggering neurodegeneration and AD onset in older age. Furthermore, corroborating evidence from various animal model studies and human case reports suggests that AD can be potentially transmissible.

Dural repair following an osteoplastic craniotomy presents significant challenges, necessitating an optimal dural substitute to avoid complications and ensure successful patient outcomes when primary dural closure is not possible. Ideal substitutes provide a scaffold for fibroblast migration and implantation, which are essential for achieving postoperative dural sealing and watertightness. However, such a substitute seldom exists, underscoring the importance of choosing appropriate materials for dural repair to reduce the risks of postoperative complications, including iatrogenic prion contamination that may promote intracranial amyloid transmission. Available dural substitutes are categorized into autologous, allogeneic, and xenogeneic transplants, as well as organic, synthetic, and composite polymer grafts. While each category offers specific benefits, many disadvantages persist, including the risks of prion-like amyloid protein deposition, particularly spreading iatrogenic Creutzfeldt-Jakob disease. These risks have historically been associated with the use of cadaveric dura grafts and prion-contaminated surgical instruments, necessitating safer replacement materials and enhanced sterilization protocols. This narrative review addresses the critical challenges of dural repair following cranial surgery, proposing innovative directions that include the use of composite materials and emerging technologies, such as 3D printing. Through a narrative review, the evaluation of traditional and advanced dural substitutes is provided, summarizing the advantages and limitations of currently available dural substitutes. In conclusion, the ideal dural substitute should closely replicate the natural structure of the dura, support tissue regeneration, and prevent postoperative complications such as cerebrospinal fluid leakage and intracranial iatrogenic amyloid transmission, thereby ensuring optimal patient outcomes and recovery.

We report a case of iatrogenic Creutzfeldt-Jakob disease (iCJD) after a 48.3-year incubation period in a patient treated with cadaveric human growth hormone. iCJD was pathologically confirmed; genetic analysis was negative for pathogenic mutations. Clinicians should consider iCJD in patients with progressive neurologic signs who had received cadaveric human growth hormone treatment.