Obstructive sleep apnea (OSA) subjects undergo multiple blockages of the upper airway, with continued diaphragmatic efforts to breath during sleep, resulting in hypoxic episodes, resulting in brain injury, including white matter damage in various regions.^1,2 The tissue injury, including dysfunctional myelin and glial cells, may contribute to deposition of iron in those areas. Iron is an essential component for synthesis of neurotransmitters and myelin function, but excess iron can create free radicals and elevate oxidative stress, leading to neurodegeneration on the surrounding tissue.³ However, the levels and distribution of regional brain iron loads in OSA subjects is unclear. Brain iron can be assessed by T2*-relaxometry procedures, and T2*-relaxation values are the inverse of R2* values, which demonstrate positive correlations with iron content. T2*-relaxometry procedures have been used to evaluate iron levels in various conditions where iron influences the condition, and may be useful to examine OSA subjects.⁴ Our aim was to examine regional iron deposition in OSA, compared to control subjects using T2*-relaxometry procedures. We hypothesized that T2*-relaxometry procedures will show altered regional iron deposition in multiple brain sites in OSA, reflected as higher R2* values, compared to control subjects.The R2* maps from the multiple echo T2*weighted images can be estimated by employing the following equation: $$$R2* = -\frac{\sum_{n=2}^{N}\frac{I_{n}}{I_{1}}*(TE_{n}-TE_{1})}{\sum_{n=2}^{N}(TE_{n}-TE_{1})^{2}}$$$ Where N is number of echo times, $$$I_{n}$$$ is T2*-weighted image at n^th echo time and $$$I_{1}$$$ is signal intensity of T2*-weighted image at first echo time.We examined 19 OSA (age, 49.8±8.4 years; body-mass-index, 33.4±7.9 kg/m²; 14 male; apnea-hypopnea index, 43.1±33.4 events/hour) and 28 control subjects (age, 45.3±9.5 years; body-mass-index (BMI), 24.8±6.9 kg/m²; 17 male). All OSA subjects were diagnosed via overnight polysomnography with at least moderate severity (AHI ≥ 15 events/hour), were treatment-naive, and recruited from the UCLA sleep disorders laboratory. Control subjects were healthy, without taking any medications that might alter brain tissue, and were recruited from the university hospital and neighboring area. All procedures were approved by the Institutional Review Board, and subjects provided written informed consent prior to the study. Brain imaging studies were performed using a 3.0-Tesla MRI scanner (Magnetom Tim-Trio; Siemens). T2*-weighted imaging was performed using a gradient-echo pulse sequence with multiple echo times (TR = 1800 ms; TEs = 5, 12, 20, and 30 ms; flip-angle = 18°; matrix-size = 256×256; FOV = 230×230 mm; slice-thickness = 3.6 mm). Using T2*-weighted images from different TEs, R2*maps were calculated voxel-by-voxel with multi-exponential curve fitting described above.. We normalized the R2* maps to Montreal Neurological Institute (MNI) space, using unified segmentation, and smoothed (Gaussian kernel, 10 mm). T2*-weighted images of control subjects were also normalized to MNI space for background images. The smoothed R2* maps were compared voxel-by-voxel between groups using ANCOVA (covariates: gender, age; SPM12, uncorrected p < 0.005). Brain clusters with significant differences between groups were overlaid onto background images for structural identification.No significant differences in gender (p = 0.28) or age (p = 0.16), appeared between groups. However, BMI significantly differed between groups (p < 0.0001). Multiple brain areas in OSA showed increased R2* values over control subjects (Fig. 1). No brain sites showed decreased R2* values in OSA, compared to control subjects. Brain areas that showed increased R2* values in OSA included the bilateral insular, temporal, parietal, and anterior cingulate cortices, and cingulum bundle, and cerebellar regions. Using the assumption that R2* values are indicative of iron presence, regional brain iron deposition is significantly increased in OSA over control subjects. The increased iron content appeared in brain areas that showed tissue injury previously, appeared predominately in white matter, and included the insular, parietal, cingulate and cingulum bundle, temporal, and cerebellar sites. The pathological mechanisms for excess iron deposition in OSA subjects may include accumulation from neural and white matter injury, including myelin and glial dysfunction, and may accelerate tissue degeneration in the condition. These findings may suggest means for intervention to lessen neural injury associated with OSA (responsible for numerous co-morbidities in the condition), by interfering with the iron processes exacerbating the injury.These data suggest that T2*-relaxometry can be used to examine regional brain iron load in OSA subjects.