Mindfulness—an attentive non-judgmental focus on present experiences—is increasingly incorporated in psychotherapeutic treatments as a skill fostering emotion regulation. Neurobiological mechanisms of actively induced emotion regulation are associated with prefrontally mediated down-regulation of, for instance, the amygdala. We were interested in neurobiological correlates of a short mindfulness instruction during emotional arousal. Using functional magnetic resonance imaging, we investigated effects of a short mindfulness intervention during the cued expectation and perception of negative and potentially negative pictures (50% probability) in 24 healthy individuals compared to 22 controls. The mindfulness intervention was associated with increased activations in prefrontal regions during the expectation of negative and potentially negative pictures compared to controls. During the perception of negative stimuli, reduced activation was identified in regions involved in emotion processing (amygdala, parahippocampal gyrus). Prefrontal and right insular activations when expecting negative pictures correlated negatively with trait mindfulness, suggesting that more mindful individuals required less regulatory resources to attenuate emotional arousal. Our findings suggest emotion regulatory effects of a short mindfulness intervention on a neurobiological level.

THE CYP46 GENE encodes cholesterol 24-hydroxylase, the rate-limiting enzyme for cholesterol removal from the brain.^1-3 Cholesterol 24-hydroxylase mediates the hydroxylation of brain cholesterol to 24-hydroxycholesterol that can be transported readily through the blood-brain barrier.⁴ Because depletion of brain cholesterol levels reduces the generation of β-amyloid peptides (Aβ),^5,6 and because cholesterol-lowering drugs may reduce the risk of dementia,^7,8 we tested whether polymorphisms of CYP46 are associated with brain β-amyloid load in humans by measuring the sequential pattern of β-amyloid deposition in the medial temporal lobe. Brain β-amyloid deposits contain large amounts of Aβ₄₂. Consequently, we next tested whether CYP46 genotypes affected levels of Aβ₄₂ in cerebrospinal fluid (CSF) obtained from patients with mild to moderate Alzheimer disease (AD).