In recent decades, deep brain stimulation (DBS) has been extensively studied due to its reversibility and significantly fewer side effects. DBS is mainly a symptomatic therapy, but the stimulation of subcortical areas by DBS is believed to affect the cytoarchitecture of the brain, leading to adaptability and neurogenesis. The neurological disorders most commonly studied with DBS were Parkinson’s disease, essential tremor, obsessive-compulsive disorder, and major depressive disorder. The most precise approach to evaluating the location of the leads still relies on the stimulus-induced side effects reported by the patients. Moreover, the adequate voltage and DBS current field could correlate with the patient’s symptoms. Implantable pulse generators are the main parts of the DBS, and their main characteristics, such as rechargeable capability, magnetic resonance imaging (MRI) safety, and device size, should always be discussed with patients. The safety of MRI will depend on several parameters: the part of the body where the device is implanted, the part of the body scanned, and the MRI-tesla magnetic field. It is worth mentioning that drug-resistant individuals may have different pathophysiological explanations for their resistance to medications, which could affect the efficacy of DBS therapy. Therefore, this could explain the significant difference in the outcomes of studies with DBS in individuals with drug-resistant neurological conditions.

Introduction: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited treatment options. Gantenerumab, a β‐amyloid–targeting monoclonal antibody, has shown mixed clinical results. With new trial data available, this updated systematic review and meta‐analysis re‐evaluates its efficacy and safety in early AD. Methods: Registered on PROSPERO (CRD420251082463) under PRISMA guidelines, we searched PubMed, Cochrane Library, and Google Scholar from inception to October 2025 for randomized trials in early AD comparing gantenerumab with placebo. A random‐effects model assessed pooled outcomes with heterogeneity ( I ² ) and sensitivity analyses. Additionally, meta‐regression and certainty of evidence using Gradepro were performed. Risk of bias was evaluated using the Cochrane tool. An Institutional Review Committee (IRC) and its Ethical Review Board (ERB) approval was not required. Results: Six trials (3103 participants: 1718 gantenerumab; 1385 placebo) were included. Gantenerumab showed no significant effect on CDR‐SB (MD = −0.07; 95% CI: −0.34–0.20; p = 0.62; I ² = 16%) but produced small improvements in FAQ (MD = −0.73; 95% CI: −1.30 to −0.17; p = 0.01; I ² = 0%) and Amyloid‐PET score (MD = −45.67; 95% CI: −88.09 to −3.24; p = 0.03; I ² = 99%). While significant statistical improvement was seen in the ADAS‐Cog13 score (MD = −0.95; 95% CI: −1.76 to −0.13; p = 0.02; I ² = 0%), the effect sizes for both FAQ and ADAS‐Cog13 fell below established MCID thresholds. MMSE and ADCS‐ADL showed no significant differences. Safety analysis revealed higher risks of ARIA‐E (RR = 5.51), ARIA‐H (RR = 1.73), and injection site reactions (RR = 2.15), with no differences in other adverse events. Conclusion: Gantenerumab significantly reduces amyloid and statistically improves select functional (FAQ) and cognitive (ADAS‐Cog13) measures in early AD; however, these changes remain below accepted MCID thresholds, indicating a lack of true clinical meaningfulness. Combined with its failure to enhance global cognition and an increased ARIA risk, routine clinical use is not supported.