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Lingford-Hughes, A.

Publications and source records attributed to Lingford-Hughes, A..

2 recordsLinked to original sources

Differences in fMRI-based functional connectivity during abstinence or interventions between heroin-dependent individuals and healthy controls

The substantial personal, societal, and economic impacts of opioid addiction drive research investigating how opioid addiction affects the brain, and whether therapies attenuate addiction-related metrics of brain function. One useful approach to characterise the effects of opioid addiction on the brain is functional connectivity (FC). FC assesses the pairwise relationship of brain region function over time. This work is a systematic narrative review of studies investigating the effect of abstinence or interventions on FC in people who are dependent on heroin (HD) and healthy controls (HC). We found that HD typically showed weaker FC between three functional networks: the Executive Control Network, Default Mode Network, and the Salience Network. Abstinence and Transcranial Magnetic Stimulation (TMS) both attenuated differences in FC between HD and HC, often by increasing FC in HD. We critically assessed the clinical relevance of these results and the impact of study methods on the robustness of study results. We concluded with practical suggestions to improve the translational potential of neuromodulatory interventions (e.g., noninvasive brain stimulation) targeting the neural correlates of opioid addiction. HighlightsO_LIFunctional connectivity (FC) informs how neural resources are organised. C_LIO_LIFC is weaker in people with heroin dependence (HD) vs healthy controls (HC) C_LIO_LIWeaker FC is observed among resting, reward, cognitive, and attentional networks. C_LIO_LIAbstinence and brain stimulation strengthen FC and reduce craving/relapse in HD. C_LIO_LIFC may be a biomarker for developing therapies for HD. C_LI

neuroscience↗

Cerebral blood flow predicts differential neurotransmitter activity

Application of metabolic magnetic resonance imaging measures such as cerebral blood flow in translational medicine is limited by the unknown link of observed alterations to specific neurophysiological processes. In particular, the sensitivity of cerebral blood flow to activity changes in specific neurotransmitter systems remains unclear. We address this question by probing cerebral blood flow in healthy volunteers using seven established drugs with known dopaminergic, serotonergic, glutamatergic and GABAergic mechanisms of action. We use a novel framework aimed at disentangling the observed effects to contribution from underlying neurotransmitter systems. We find for all evaluated compounds a reliable spatial link of respective cerebral blood flow changes with underlying neurotransmitter receptor densities corresponding to their primary mechanisms of action. The strength of these associations with receptor density is mediated by respective drug affinities. These findings suggest that cerebral blood flow is a sensitive brain-wide in-vivo assay of metabolic demands across a variety of neurotransmitter systems in humans.

neuroscience↗