Baclofen-Induced Changes in the Resting Brain Modulate Smoking Cue Reactivity: A Double-blind Placebo-controlled Functional Magnetic Resonance Imaging Study in Cigarette Smokers

Objective: Smoking cue-(SC) elicited craving can lead to relapse in SC-vulnerable individuals. Thus, identifying treatments that target SC-elicited craving is a top research priority. Reduced drug cue neural activity is associated with recovery and is marked by a profile of greater tonic (resting) activation in executive control regions, and increased connectivity between executive and salience regions. Evidence suggests the GABA-B agonist baclofen can reduce drug cue-elicited neural activity, potentially through its actions on the resting brain. Based on the literature, we hypothesize that baclofen’s effects in the resting brain can predict its effects during SC exposure. Methods: In this longitudinal, double blind, placebo-controlled neuropharmacological study 43 non-abstinent, sated treatment-seeking cigarette smokers (63% male) participated in an fMRI resting-state scan and a SC-reactivity task prior to (T1) and 3 weeks following randomization (T2; baclofen: 80 mg/day; n = 21). Subjective craving reports were acquired before and after SC exposure to explicitly examine SC-induced craving. Results: Whole-brain full-factorial analysis revealed a group-by-time interaction with greater resting brain activation of the right dorsolateral prefrontal cortex (dlPFC) at T2 in the baclofen group (BAC) (pFWEcorr = 0.02), which was associated with reduced neural responses to SCs in key cue-reactive brain regions; the anterior ventral insula and ventromedial prefrontal cortex (pFWEcorr ＜ 0.01). BAC, but not the placebo group reported decreased SC-elicited craving (p = 0.02). Conclusion: Results suggest that baclofen mitigates the reward response to SCs through an increase in tonic activation of the dlPFC, an executive control region. Through these mechanisms, baclofen may offer SC-vulnerable smokers protection from SC-induced relapse

How fleeting is fame? Collective memory for popular music

In this paper, we investigated the collective memory for popular music. To assess how well number-one hits are recognized over time, we randomly selected top songs from the last 76 years and presented them to a large sample of mostly millennial participants. In response to hearing each selection, participants were prompted to indicate whether they recognized each song. We found three distinct phases in collective memory: a steep linear drop-off in recognition for the music from this millennium, a stable plateau from the 1960s to the 1990s, and a further but more gradual drop-off for music from the 1940s and 1950s. More than half of recognition variability between songs can be accounted for by exposure as measured by Spotify play counts. We conclude that in the musical realm, fame is fleeting - but perhaps not as fleeting as previously suggested

Who remembers the Beatles? The collective memory for popular music.

How well do we remember popular music? To investigate how hit songs are recognized over time, we randomly selected number-one Billboard singles from the last 76 years and presented them to a large sample of mostly millennial participants. In response to hearing each song, participants were prompted to indicate whether they recognized it. Plotting the recognition proportion for each song as a function of the year during which it reached peak popularity resulted in three distinct phases in collective memory. The first phase is characterized by a steep linear drop-off in recognition for the music from this millennium; the second phase consists of a stable plateau during the 1960s to the 1990s; and the third phase, a further but more gradual drop-off during the 1940s and 1950s. More than half of recognition variability can be accounted for by self-selected exposure to each song as measured by its play count on Spotify. We conclude that collective memory for popular music is different from that of other historical phenomena

Associations between alcohol consumption and gray and white matter volumes in the UK Biobank

Heavy alcohol consumption has been associated with brain atrophy, neuronal loss, and poorer white matter fiber integrity. However, there is conflicting evidence on whether light-to-moderate alcohol consumption shows similar negative associations with brain structure. To address this, we examine the associations between alcohol intake and brain structure using multimodal imaging data from 36,678 generally healthy middle-aged and older adults from the UK Biobank, controlling for numerous potential confounds. Consistent with prior literature, we find negative associations between alcohol intake and brain macrostructure and microstructure. Specifically, alcohol intake is negatively associated with global brain volume measures, regional gray matter volumes, and white matter microstructure. Here, we show that the negative associations between alcohol intake and brain macrostructure and microstructure are already apparent in individuals consuming an average of only one to two daily alcohol units, and become stronger as alcohol intake increases

Associations between alcohol consumption and gray and white matter volumes in the UK Biobank.

Heavy alcohol consumption has been associated with brain atrophy, neuronal loss, and poorer white matter fiber integrity. However, there is conflicting evidence on whether light-to-moderate alcohol consumption shows similar negative associations with brain structure. To address this, we examine the associations between alcohol intake and brain structure using multimodal imaging data from 36,678 generally healthy middle-aged and older adults from the UK Biobank, controlling for numerous potential confounds. Consistent with prior literature, we find negative associations between alcohol intake and brain macrostructure and microstructure. Specifically, alcohol intake is negatively associated with global brain volume measures, regional gray matter volumes, and white matter microstructure. Here, we show that the negative associations between alcohol intake and brain macrostructure and microstructure are already apparent in individuals consuming an average of only one to two daily alcohol units, and become stronger as alcohol intake increases