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As neurosurgery has advanced technologically, more and more neurosurgical implants are being employed on an aging patient population with several comorbidities. As a result, there is a steady increase in the frequency of infections linked to neurosurgical implants, which causes serious morbidity and mortality as well as abnormalities of the skull and inadequate brain protection. We discuss infections linked to internal and external ventricular and lumbar cerebrospinal fluid drainages, neurostimulators, craniotomies, and cranioplasty in this article. Biofilms, which are challenging to remove, are involved in all implant‐associated illnesses. It takes a small quantity of microorganisms to create a biofilm on the implant surface. Skin flora bacteria are implicated in the majority of illnesses. Microorganisms that cause disruptions in wound healing make their way to the implant either during or right after surgery. In about two thirds of patients, implant‐associated infections manifest early (within the first month after surgery), whereas the remaining infections present later as a result of low‐grade infections or by direct extension from adjacent infections (per continuitatem) to the implants due to soft tissue damage. Except for ventriculo‐atrial cerebrospinal fluid shunts, neurosurgical implants are rarely infected by the haematogenous route. This research examines established and clinically validated principles that are applicable to a range of surgical specialties using implants to treat biofilm‐associated infections in orthopaedic and trauma cases. Nevertheless, there is little evidence and no evaluation in sizable patient populations to support the success of this extrapolation to neurosurgical patients. An optimal microbiological diagnostic, which includes sonicating removed implants and extending culture incubation times, is necessary for a positive result. Additionally, a strategy combining surgical and antibiotic therapy is needed. Surgical procedures involve a suitable debridement along with implant replacement or exchange, contingent on the biofilm's age and the state of the soft tissue. A protracted biofilm‐active therapy is a component of antimicrobial treatment, usually lasting 4–12 weeks. This idea is appealing because it allows implants to be changed or kept in place for a single surgical procedure in a subset of patients. This not only enhances quality of life but also lowers morbidity because each additional neurosurgical procedure increases the risk of secondary complications like intracerebral bleeding or ischemia. [ABSTRACT FROM AUTHOR]

Neuronal apoptosis is an important process of secondary brain injury which is induced by neurochemical signaling cascades after traumatic brain injury (TBI). Present study was designed to investigate whether FOS-like antigen 1 (Fra-1) is involved in the neuronal apoptosis. Western blot analysis and immunohistochemistry in a rat TBI model revealed a significant increase in the expression of Fra-1 in the ipsilateral brain cortex, which was in parallel with increase in the expression of active caspase-3. With immunofluorescence double-labeling, Fra-1 was colocalized with active caspase-3 and with NeuN, a neuronal marker. In an in vitro cell injury model, HO exposure induced cell apoptosis and reduced cell viability and at the same time, a similar increased expression of active caspase-3, p53 and Fra-1 was found in PC12 cells. Down-regulation of Fra-1 through transfection with Fra-1 siRNA remarkably elevated cell viability, reduced the expression of active caspase-3 and p53, and decreased apoptosis of PC12 cells after HO exposure. Taken together, present findings suggest that Fra-1 may be involved in the induction of neuronal apoptosis through up-regulating p53 signaling pathway and that this action may contribute to the secondary neuropathological process after TBI. [ABSTRACT FROM AUTHOR]

Background: Cerebral aneurysm is a high-risk cerebrovascular disease with a poor prognosis, potentially linked to multiple factors. This study aims to explore the association between mitochondrial-associated proteins and the risk of cerebral aneurysms using Mendelian randomization (MR) methods., Methods: We used GWAS summary statistics from the IEU Open GWAS project for mitochondrial-associated proteins and from the Finnish database for cerebral aneurysms (uIA, aSAH). The association between mitochondrial-associated exposures and cerebral aneurysms was evaluated using MR-Egger, weighted mode, IVW, simple mode and weighted median methods. Reverse MR assessed reverse causal relationship, while sensitivity analyses examined heterogeneity and pleiotropy in the instrumental variables. Significant causal relationship with cerebral aneurysms were confirmed using FDR correction., Results: Through MR analysis, we identified six mitochondrial proteins associated with an increased risk of aSAH: AIF1 (OR: 1.394, 95% CI: 1.109-1.752, p  = 0.0044), CCDC90B (OR: 1.318, 95% CI: 1.132-1.535, p  = 0.0004), TIM14 (OR: 1.272, 95% CI: 1.041-1.553, p  = 0.0186), NAGS (OR: 1.219, 95% CI: 1.008-1.475, p  = 0.041), tRNA PusA (OR: 1.311, 95% CI: 1.096-1.569, p  = 0.003), and MRM3 (OR: 1.097, 95% CI: 1.016-1.185, p  = 0.0175). Among these, CCDC90B, tRNA PusA, and AIF1 demonstrated a significant causal relationship with an increased risk of aSAH (FDR q  < 0.1). Three mitochondrial proteins were associated with an increased risk of uIA: CCDC90B (OR: 1.309, 95% CI: 1.05-1.632, p  = 0.0165), tRNA PusA (OR: 1.306, 95% CI: 1.007-1.694, p  = 0.0438), and MRM3 (OR: 1.13, 95% CI: 1.012-1.263, p  = 0.0303). In the reverse MR study, only one mitochondrial protein, TIM14 (OR: 1.087, 95% CI: 1.004-1.177, p  = 0.04), showed a causal relationship with aSAH. Sensitivity analysis did not reveal heterogeneity or pleiotropy. The results suggest that CCDC90B, tRNA PusA, and MRM3 may be common risk factors for cerebral aneurysms (ruptured and unruptured), while AIF1 and NAGS are specifically associated with an increased risk of aSAH, unrelated to uIA. TIM14 may interact with aSAH., Conclusion: Our findings confirm a causal relationship between mitochondrial-associated proteins and cerebral aneurysms, offering new insights for future research into the pathogenesis and treatment of this condition., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Wang, Wang, Niu, Zhang, Yang, Hou and Lin.)