Humans typically lack awareness that they are dreaming while dreaming. However, at times a remarkable exception occurs and reflective consciousness can be regained while dreaming, referred to as lucid dreaming. While most individuals experience lucid dreams rarely there is substantial variance in lucid dream frequency. The neurobiological basis of lucid dreaming is unknown, but evidence points to involvement of anterior prefrontal cortex (aPFC) and parietal cortex. This study evaluated the neuroanatomical/neurofunctional correlates of frequent lucid dreams and specifically whether functional connectivity of aPFC is associated with frequent lucid dreams. We analyzed structural and functional magnetic resonance imaging from an exceptional sample of fourteen individuals who reported ≥3 lucid dreams/week and a control group matched on age, gender and dream recall that reported ≤1 lucid dream/year. Compared to controls, the frequent lucid dream group showed significantly increased resting-state functional connectivity between left aPFC and bilateral angular gyrus, bilateral middle temporal gyrus and right inferior frontal gyrus, and higher node degree and strength in left aPFC. In contrast, no significant differences in brain structure were observed. Our results suggest that frequent lucid dreaming is associated with increased functional connectivity between aPFC and temporoparietal association areas, regions normally deactivated during sleep. Compared to controls, the frequent lucid dream group showed significantly increased resting-state functional connectivity between left aPFC and bilateral angular gyrus, bilateral middle temporal gyrus and right inferior frontal gyrus, and higher node degree and strength in left aPFC. In contrast, no significant differences in brain structure were observed. Our results suggest that frequent lucid dreaming is associated with increased functional connectivity between aPFC and temporoparietal association areas, regions normally deactivated during sleep. The prefrontal cortex (particularly the lateral and rostrolateral regions), parietal cortex and lateral middle temporal cortex show low regional cerebral blow flow (rCBF) throughout sleep, including during REM sleep 13 – 15 , the stage of sleep most strongly associated with dreaming. Hypoactivity of these regions has been postulated to underlie the diminished self-awareness and volitional control during dreaming 15 , 16 . In contrast to these functional changes, we did not observe any differences in brain structure (gray matter density) in any brain area between groups (c.f. ref. 30 ). Furthermore, no differences were observed between frequent lucid dream and control groups in behavioral or questionnaire measures of working memory capacity, prospective memory, mind-wandering frequency or trait mindfulness. Our results converge with a recent fMRI case study of lucid dreaming, which found that a highly similar network of brain areas increased fMRI BOLD signal during lucid compared to baseline REM sleep, including bilateral aPFC, bilateral ITG/MTG, and bilateral medial/lateral parietal cortex (including AG) 9 . These same brain areas, particularly aPFC and IPL/AG, show reduced regional cerebral blood flow (rCBF) 13 , 14 , 39 during REM sleep compared to waking (see ref. 15 for a review). Hypoactivity of these regions coupled with preserved or increased activity in limbic/paralimbic structures and extrastriate cortices has been postulated to facilitate a mode of brain function conducive to hallucinatory dream mentation but diminished higher-order consciousness/self-awareness 40 , 41 . The current results suggest that increased functional integrity during wakefulness between aPFC and temporoparietal association areas—all regions that show suppressed activity in REM sleep and increased activity during lucid REM sleep—is associated with the tendency to have frequent lucid dreams. Lucid dreaming and brain connectivity Becoming lucid during REM sleep dreaming involves making an accurate metacognitive judgment about the state of consciousness one is in, often by recognizing that the correct explanation for an anomaly in the dream is that one is dreaming 1 , 2 . Future longitudinal training studies would be valuable in order to evaluate within-subject changes in While we did not find evidence in support of a relationship between these variables and spontaneous frequent lucid dreams, it is worth noting that the relation between lucid dreaming and working memory has been discussed primarily in the context of successfully being able to “activate the pre-sleep intention to recognize that one is dreaming” during a dream 2 , and the relation to prospective memory is mostly considered in the context of learning to have lucid dreams by remembering to recognize that one is dreaming. 69 for a review), pro-cholinergic drugs in general tend to increase frontoparietal activity in conditions in which these areas show low baseline activation, which is thought to reflect increased attentional-executive functions 69 . Given that frontoparietal activity is typically suppressed during REM sleep, an intriguing follow-up to these findings based on the current results would be to examine whether AChEIs, and galantamine in particular, may facilitate lucid dreaming through increasing activation within the network of fronto-temporo-parietal areas observed here. In summary, it remains unclear whether electrical brain stimulation techniques could be effective for inducing lucid dreams (see refs 19 , 62 for further discussion). Nevertheless, given the current findings, stimulation of aPFC and temporoparietal association areas appears to be a worthwhile direction for future research attempting to induce lucid dreaming. Future studies might consider testing a wider range of stimulation parameters, particularly applied to aPFC, as well as combining stimulation with training in the appropriate attentional set for lucid dream induction.