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See Gratwicke and Foltynie (doi:) for a scientific commentary on this article.Cognitive impairments in Parkinson’s disease show variable onset, severity and progression. Ray et al. demonstrate that the future cognitive status of newly diagnosed patients can be predicted from the volume of the nucleus basalis of Meynert, with implications for the development of interventions for cognitive decline in Parkinson’s disease dementia.

Impulsivity is a complex behaviour composed of different domains encompassing behavioural disinhibition, risky decision-making and delay discounting abnormalities. To investigate regional brain correlates between levels of individual impulsivity and grey matter volume, we performed voxel-based morphometric correlation analysis in 34 young, healthy subjects using impulsivity scores measured with Barratt Impulsivity Scale-11 and computerized Kirby's delay discounting task. The VBM analysis showed that impulsivity appears to be reliant on a network of cortical (medial prefrontal cortex and dorsolateral prefrontal cortex) and subcortical (ventral striatum) structures emphasizing the importance of brain networks associated with reward related decisionmaking in daily life as morphological biomarkers for impulsivity in a normal healthy population. While our results in healthy volunteers may not directly extend to pathological conditions, they provide an insight into the mechanisms of impulsive behaviour in patients with abnormalities in prefrontal/frontal-striatal connections, such as in drug abuse, pathological gambling, ADHD and Parkinson's disease.

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The subthalamic nucleus (STN) is a key node in the network that supports response inhibition. It is suggested that the STN rapidly inhibits basal ganglia activity, to pause motor output during conflict until an appropriate motor plan is ready. Here, we recorded neural activity during a Stroop task from deep brain stimulation electrodes implanted in the human STN. We intended to determine whether cognitive psychological phenomena such as the Stroop effect can be explained via mechanisms of response inhibition involving the STN, or whether higher cognitive centers are alone responsible. We show stimulus-driven desychronization in the beta band (15-35 Hz) that lasts throughout the verbal response, in keeping with the idea that beta-band synchrony decreases to allow motor output to occur. During incongruent trials-in which response times were elongated due to the Stroop effect-a resynchronization was seen in the beta band before response. Crucially, in the incongruent trials during which the participant was unable to withhold the prepotent response, this resynchronization occurred after response onset. We suggest that this beta-band resynchronization pauses the motor system until conflict can be resolved.

The pedunculopontine nucleus is composed of cholinergic and non-cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post-mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man.

Introduction Increasing imaging evidence supports the role of neuroinflammation in dementia pathogenesis. Despite this, the spatial association within the brain has not been comprehensively meta-analysed. Methods We searched literature databases for case-control studies examining the levels of translocator protein (TSPO) levels, representing neuroinflammation, in region of interest analyses between healthy controls and mild cognitive impairment (MCI) or Alzheimer's disease (AD) subjects. Standardised mean difference effect sizes were calculated and results meta-analysed using randomeffects models. Results The literature search identified 28 studies for inclusion, covering 37 different brain regions of interest. Compared to healthy controls, AD subjects had widespread increased TSPO levels throughout the brain, with the largest effects seen in fronto-temporo-parieto-occipital regions. MCI subjects also had increased TSPO levels, mainly within the neocortex, however, the effects were more modest. Discussion Neuroinflammation effect sizes increases and disperses from MCI to AD, relative to healthy controls.