Glioblastoma multiforme (GBM), a WHO grade 4 glioma, is the most common and aggressive primary brain tumor, characterized by rapid progression and poor prognosis. The heterogeneity of GBM complicates diagnosis and treatment, driving research into molecular biomarkers that can offer insights into tumor behavior and guide personalized therapies. This review explores recent advances in molecular biomarkers, highlighting their potential to improve diagnosis and treatment outcomes in GBM patients. Key biomarkers such as MGMT promoter methylation, IDH1/2 mutations, EGFR amplification, and TERT promoter mutations, etc., are examined for their roles in prognosis, therapeutic response, and tumor classification. While molecular biomarkers offer valuable insights for tailoring GBM treatments, their clinical application is hindered by tumor heterogeneity, dynamic genetic evolution, and the lack of standardized testing methods. Future research should aim to confirm new biomarkers and incorporate them into regular clinical practice to improve prognosis and treatment choices. Advances in genomic and proteomic technologies, along with consistent biomarker detection, could transform GBM care and enhance patient outcomes.

Deep brain stimulation (DBS) is an established therapy for motor symptom management in Parkinson’s disease (PD), yet emerging evidence suggests that its effects may extend beyond functional circuit modulation to include cellular and molecular mechanisms with potential neuroprotective significance. This review synthesizes current evidence on the neuroprotective mechanisms of DBS, with an emphasis on preclinical and clinical studies that highlight its effects on neuronal survival, trophic support, oxidative stress, inflammation, synaptic plasticity, and network homeostasis. Preclinical data indicate that DBS reduces dopaminergic neuron degeneration, enhances brain-derived neurotrophic factor (BDNF) signaling, preserves mitochondrial function, attenuates neuroinflammation, and fosters synaptic remodeling. Clinical studies provide convergent, though less definitive, evidence from imaging, fluid biomarkers, and long-term outcomes supporting potential disease-modifying effects. These findings underscore a shift in the conceptualization of DBS from purely symptomatic relief toward modulation of underlying pathogenic processes. DBS holds promise as a neuroprotective therapy for PD, but critical gaps remain in validating these mechanisms in patients. Future directions include the development of biomarker-driven longitudinal studies, refinement of adaptive stimulation strategies, integration with adjunctive disease-modifying strategies, and exploration of personalized approaches based on molecular and network signatures. By bridging mechanistic understanding with translational innovation, DBS may evolve into a precision therapy capable of altering the progression trajectory of PD.