Neuroscience
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1H magnetic resonance imaging (MRI) has established itself as a key diagnostic technique, affording the visualization of brain anatomy, blood flow, activity and connectivity. The detection of other atoms (e.g. 19F, 23Na, 31P), so called hetero-nuclear MRI and spectroscopy (MRS), provides investigative avenues that complement and extend the richness of information that can be gained from 1H MRI. Especially 19F MRI is increasingly emerging as a multi-nuclear (1H/19F) technique that can be exploited to visualize cell migration and trafficking. ⋯ Further methodological advances that accelerate signal acquisition (e.g. compressed sensing, cryogenic coils) are required to expand the applications of 19F MR imaging to, for instance, determine the regional pharmacokinetics of novel fluorine-based drugs. Improvements in 19F signal detection and localization, combined with the development of novel sensitive probes, will increase the utility of these multi-nuclear studies. These advances will provide new insights into cellular and molecular processes involved in neurodegenerative disease, as well as the mode of action of pharmaceutical compounds.
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The history of magnetic resonance imaging (MRI) is closely linked to our improved understanding of memory systems, be it in normal functioning or altered due to pathologies. Over the years, brain imaging using MRI has moved from simple volumetric imaging to complex analysis using multiple sequences, allowing the measurement of microstructural integrity and brain activation through a dedicated task or at rest. This review aims at showing how the advent and evolution of magnetic resonance imaging has shaped a better understanding of memory and brain function in humans. We will give a brief overview on the history of MRI, how its evolution brought about concomitant improvement in our understanding of memory systems, going from final-stage observation to risk-prediction via the detection of subtle, but important, alterations in normal brain functioning.
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Age-related changes may affect the performance during fast walking speed. Although, several studies have been focused on the contribution of the prefrontal cortex (PFC) during challenging walking tasks, the neural mechanism underling fast walking speed in older people remain poorly understood. Therefore, the aim of this study was to investigate the influence of aging on PFC activity during overground walking at preferred and fast speeds. ⋯ Older adults significantly increased activity in the left PFC from the preferred to fast walking condition whereas young adults had similar levels of PFC activity across conditions. Our findings suggest that older adults need to recruit additional prefrontal cognitive resources to control walking, indicating a compensatory mechanism. In addition, left PFC seems to be involved in the modulation of gait speed in older adults.
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During adolescence, heavy binge-like ethanol consumption can lead to frontocortical structural and functional impairments. These impairments are likely driven by adolescence being a critical time point for maturation of brain regions associated with higher-order cognitive functioning. Rodent models of heavy binge-like ethanol exposure show consistent disruptions to the typical development of the prefrontal cortex (PFC). ⋯ However, AIE spared performance on the spatial memory task and on an operant reversal task. In a second study, Golgi-Cox staining determined that AIE increased apical dendritic complexity in the OFC, with sex influencing whether the increase in branching occurred near or away from the soma. Spine density or maturity was not affected, likely compensating for a disruption in neurotransmitter function following AIE.