Medical Conditions Linked to Atherosclerosis Are Associated With Magnified Cortical Thinning in Individuals With Alcohol Use Disorders.

AIMS: Magnetic resonance imaging (MRI) studies report widespread cortical thinning in individuals with alcohol use disorder (AUD), but did not consider potential effects of pro-atherogenic conditions such as hypertension, type 2 diabetes mellitus, hepatitis C seropositivity and hyperlipidemia on cortical thickness. The conditions are associated with regional cortical thinning in those without AUD. We predicted that individuals with concurrent AUD and pro-atherogenic conditions demonstrate the greatest regional cortical thinning in areas most vulnerable to decreased perfusion. METHODS: Treatment-seeking individuals with AUD (n = 126) and healthy controls (CON; n = 49) completed a 1.5 T MRI study. Regional cortical thickness was quantitated via FreeSurfer. Individuals with AUD and pro-atherogenic conditions (Atherogenic+), AUD without pro-atherogenic conditions (Atherogenic-) and CON were compared on regional cortical thickness. RESULTS: Individuals with AUD showed significant bilateral cortical thinning compared to CON, but Atherogenic+ demonstrated the most widespread and greatest magnitude of regional thinning, while Atherogenic- had reduced thickness primarily in anterior frontal and posterior parietal lobes. Atherogenic+ also showed a thinner cortex than Atherogenic- in lateral orbitofrontal and dorso/dorsolateral frontal cortex, mesial and lateral temporal and inferior parietal regions. CONCLUSIONS: Our results demonstrate significant bilateral cortical thinning in individuals with AUD relative to CON, but the distribution and magnitude were influenced by comorbid pro-atherogenic conditions. The magnitude of cortical thinning in Atherogenic+ strongly corresponded to cortical watershed areas susceptible to decreased perfusion, which may result in morphometric abnormalities. The findings indicate that pro-atherogenic conditions may contribute to cortical thinning in those seeking treatment for AUD.

Low CD4 nadir linked to widespread cortical thinning in adults living with HIV.

BACKGROUND: The history of immune suppression, especially CD4 nadir, has been shown to be a strong predictor of HIV-associated neurocognitive disorders (HAND). However, the potential mechanism of this association is not well understood. METHODS: High resolution structural MRI images and neuropsychological data were obtained from fifty-nine HIV+ adults (mean age, 56.5 ± 5.8) to investigate the correlation between CD4 nadir and cortical thickness. RESULTS: Low CD4 nadir was associated with widespread cortical thinning, especially in the frontal and temporal regions, and global mean cortical thickness correlated with CD4 nadir. In addition, worse global neurocognitive function was associated with bilateral frontal cortical thinning, and the association largely persisted (especially in the left frontal cortex) in the subset of participants who did not meet HAND criteria. CONCLUSIONS: These results suggest that low CD4 nadir may be associated with widespread neural injury in the brain, especially in the frontal and temporal regions. The diffuse neural injury might contribute to the prevalence and the phenotypes of HAND, as well as the difficulty treating HAND due to a broad network of brain regions affected. Low CD4 nadir related neural injury to the frontal cortex might contribute to subtle neurocognitive impairment/decline, even in the absence of HAND diagnosis.