Obesity is a systemic metabolic disorder characterized by chronic low-grade inflammation and insulin resistance, with growing evidence indicating that the brain represents a primary and particularly vulnerable target organ. Beyond peripheral metabolic consequences, obesity induces region-specific structural, functional, and biochemical alterations within the central nervous system, contributing to cognitive impairment, dysregulated energy homeostasis, and increased susceptibility to neurodegenerative diseases. This narrative review examines key neurometabolic and neuroinflammatory mechanisms underlying obesity-related brain vulnerability, including downstream neuroinflammation, impaired insulin signaling, mitochondrial dysfunction, oxidative stress, blood–brain barrier disruption, and impaired brain clearance mechanisms. These processes preferentially affect frontal and limbic networks involved in executive control, reward processing, salience detection, and appetite regulation. Advanced neuroimaging has substantially refined our understanding of these mechanisms. Magnetic resonance spectroscopy provides unique in vivo insight into early neurometabolic alterations that may precede irreversible structural damage and is complemented by diffusion imaging, volumetric MRI, functional MRI, cerebral perfusion imaging, and positron emission tomography. Together, these complementary modalities reveal microstructural, network-level, structural, hemodynamic, and molecular alterations associated with obesity-related brain vulnerability and support the concept that such brain dysfunction is dynamic and potentially modifiable. Integrating neurometabolic and multimodal neuroimaging biomarkers with metabolic and clinical profiling may improve early risk stratification and guide preventive and therapeutic strategies aimed at preserving long-term brain health in obesity.

Background and Objectives: Obesity-related chronic inflammation may lead to neuroinflammation and neurodegeneration. This study aimed to evaluate the neurometabolic profile of obese patients using cerebral multivoxel magnetic resonance spectroscopy (mvMRS) and assess correlations between brain metabolites and obesity markers, including body mass index (BMI), waist circumference, waist-hip ratio, body fat percentage, and indicators of metabolic syndrome (e.g., triglycerides, HDL cholesterol, fasting blood glucose, insulin, and insulin resistance index (HOMA-IR)). Materials and Methods: This prospective study involved 100 participants, stratified into two groups: 50 obese individuals (BMI ≥ 30 kg/m²) and 50 controls (18.5 ≤ BMI < 25 kg/m²). Anthropometric measurements, body fat percentage, and biochemical markers were evaluated. All subjects underwent long- and short-echo mvMRS analysis of the frontal and parietal supracallosal subcortical and deep white matter, as well as the cingulate gyrus, analyzing NAA/Cr, Cho/Cr, and mI/Cr ratios, along with absolute concentrations of NAA and Cho. Results: Obese participants exhibited significantly decreased NAA/Cr and Cho/Cr ratios in the deep white matter of the right cerebral hemisphere (p < 0.001), while absolute concentrations of NAA and Cho did not differ significantly between groups (p > 0.05). NAA levels showed negative correlations with more reliable obesity parameters (waist circumference and waist-to-hip ratio) but not with BMI, particularly in the deep frontal white matter and dorsal anterior cingulate gyrus of the left cerebral hemisphere. Notably, insulin demonstrated a significant negative impact on NAA (ρ = −0.409 and ρ = −0.410; p < 0.01) and Cho levels (ρ = −0.403 and ρ = −0.392; p < 0.01) at these locations in obese individuals. Conclusions: Central obesity and hyperinsulinemia negatively affect specific brain regions associated with cognitive and emotional processing, while BMI is not a reliable parameter for assessing brain metabolism.

Background and Objectives: The pineal gland is a neuroendocrine structure whose function can be disrupted in patients with malignancies. This study examines the differences in pineal gland volume between oncology patients and healthy controls, as well as the relationship between volume and the duration of chemotherapy. Materials and Methods: A retrospective study included 400 participants, divided into two groups: 200 oncology patients and 200 healthy controls. The pineal gland volume was measured using MRI scans, utilizing T1-sagittal, T2-coronal/axial sections, and post-contrast 3D T1W MPRAGE tomograms. The volume was calculated based on the ellipse approximation formula: V = (L × H × W)/2. The study analyzed the relationships between pineal gland volume and factors such as age, sex, primary tumor origin, and the duration of chemotherapy. Results: The pineal gland volume was significantly smaller in oncology patients in comparison with the healthy controls (p < 0.001). The average volume in oncology patients was 32.41 ± 16.79 mm³, whereas in healthy controls, it was 59.26 ± 29.99 mm³. A significantly smaller pineal gland volume was observed in patients with malignancies, regardless of sex, with no notable differences between groups. Age also did not significantly influence gland volume (p > 0.05). The primary tumor site did not significantly influence gland volume (p > 0.05). A moderate positive correlation was observed between the duration of chemotherapy and pineal gland volume (ρ = 0.322; p = 0.007). Conclusions: The pineal gland showed reduced volume in oncology patients compared to controls. The observed positive correlation with chemotherapy duration should be interpreted cautiously and may reflect survivorship bias rather than direct treatment effects.

Introduction. Neuromyelitis optica spectrum disorder (NMOSD) represents an immune-mediated neuroinflammatory syndrome, classified as a separate entity after the discovery of aquaporin-4 immunoglobulin G (anti-AQP4-IgG). The magnetic resonance neuroimaging spectrum of NMOSD classically consists of bilateral optic neuritis and longitudinally extensive transverse myelitis (LETM), recently broadened with lesions in area postrema, diencephalon, brainstem and cerebellum, and extensive cord atrophy. Case report. The case presents an anti-AQP4 autoantibody-positive 65-year-old female patient who initially presented with underestimated LETM and developed multiple cerebral and cerebellar lytic demyelinating lesions associated with acute long segment op-tic nerve involvement two years later. Two new imaging findings were described in this case: the involvement of a complete cross-sectional area of pons and microhemorrhage in the pons and corpus callosum. Conclusion. Raising suspicion of NMOSD is of crucial importance in cases with isolated LETM in order to prevent relapses in anti-AQP4-IgG positive cases and improve patient outcomes and recovery.