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Greg J Elder,1 Mark A Wetherell,2 Thomas V Pollet,2 Nicola L Barclay,3 Jason G Ellis1 1Northumbria Sleep Research Laboratory, Northumbria University, Newcastle Upon Tyne, UK; 2Department of Psychology, Northumbria University, Newcastle Upon Tyne, UK; 3Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UKCorrespondence: Greg J ElderNorthumbria Sleep Research Laboratory, Northumbria University, Newcastle Upon Tyne NE1 8ST, UKTel +44 191 227 3241Email g.elder@northumbria.ac.ukPurpose: Stress is associated with subjective and objective sleep disturbances; however, it is not known whether stress disrupts sleep and relevant physiological markers of stress immediately after it is experienced. The present study examined whether demand, in the form of cognitive tasks, disrupted sleep and the cortisol awakening response (CAR), depending on whether it was experienced or just anticipated.Participants and Methods: Subjective and objective sleep was measured in 22 healthy adults on three nights (Nights 0– 2) in a sleep laboratory using sleep diaries and polysomnography. Saliva samples were obtained at awakening, +15, +30, +45 and +60 minutes on each subsequent day (Day 1– 3) and CAR measurement indices were derived: awakening cortisol levels, the mean increase in cortisol levels (MnInc) and total cortisol secretion (AUCG). On Night 1, participants were informed that they were required to complete a series of demanding cognitive tasks within the sleep laboratory during the following day. Participants completed the tasks as expected or unexpectedly performed sedentary activities.Results: Compared to the no-demand group, the demand group displayed significantly higher levels of state anxiety immediately completing the first task. There were no subsequent differences between the demand and no-demand groups in Night 2 subjective sleep continuity, objective sleep continuity or architecture, or on any Day 3 CAR measure.Conclusion: These results indicate that sleep and the CAR are not differentially affected depending on whether or not an anticipated stressor is then experienced. This provides further evidence to indicate that the CAR is a marker of anticipation and not recovery. In order to disrupt sleep, a stressor may need to be personally relevant or of a prolonged duration or intensity.Keywords: stress, cortisol, polysomnography, sleep, anticipation

Objectives Several cholinergic nuclei, and in particular the nucleus basalis of Meynert, are localised to the substantia innominata in the basal forebrain. These nuclei provide major cholinergic innervation to the cerebral cortex and hippocampus, and have an essential role in cognitive function. The aim of this study was to investigate volumetric grey matter (GM) changes in the substantia innominata from structural T1 images in Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and healthy older participants using voxel‐based morphometry. Methods Participants (41 DLB, 47 AD and 39 controls) underwent 3 T T1 magnetic resonance imaging and cognitive assessments. Voxel‐based morphometry analysis used SPM8 with a substantia innominata brain mask to define the subspace for voxel GM analyses. Group differences, and selected behavioural and clinical correlates, were assessed. Results Compared with that in controls, bilateral GM loss in the substantia innominata was apparent in both AD and DLB. Relative to controls, significant bilateral GM loss in the substantia innominata was observed in DLB and AD. In DLB, significant associations were also observed between substantia innominata GM volume loss, and the levels of cognitive impairment and severity of cognitive fluctuations. Conclusions Relative to that controls, atrophy of the substantia innominata was apparent in DLB and AD, and is associated with specific clinical manifestations in DLB. © 2016 The Authors. International Journal of Geriatric Psychiatry Published by John Wiley & Sons Ltd.

Objective Sleep problems and depression are common symptoms in dementia with Lewy bodies (DLB), where patients typically experience subjectively poor sleep quality, fatigue and excessive daytime sleepiness. However, whilst sleep disturbances have been linked to depression, this relationship has not received much attention in DLB. The present cross‐sectional study addresses this by examining whether depressive symptoms are specifically associated with subjective sleep quality and daytime sleepiness in DLB, and by examining other contributory factors. Methods DLB patients (n = 32) completed the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS) and the 15‐item Geriatric Depression Scale (GDS‐15). Motor and cognitive functioning was also assessed. Pearson correlations were used to assess the relationship between GDS‐15, ESS and PSQI scores. Results GDS‐15 scores were positively associated with both ESS (r = 0.51, p

OBJECTIVE: Lewy body dementias (LBD) include both dementia with Lewy bodies (DLB) and Parkinson's disease with dementia (PDD), and the differentiation of LBD from other neurodegenerative dementias can be difficult. Currently, there are few biomarkers which might assist early diagnosis, map onto LBD symptom severity, and provide metrics of treatment response. Traditionally, biomarkers in LBD have focussed on neuroimaging modalities; however, as biomarkers need to be simple, inexpensive and non-invasive, neurophysiological approaches might also be useful as LBD biomarkers.\ud \ud METHODS: In this review, we searched PubMED and PsycINFO databases in a semi-systematic manner in order to identify potential neurophysiological biomarkers in the LBDs.\ud \ud RESULTS: We identified 1491 studies; of these, 37 studies specifically examined neurophysiological biomarkers in LBD patients. We found that there was substantial heterogeneity with respect to methodologies and patient cohorts.\ud \ud CONCLUSION: Generally, many of the findings have yet to be replicated, although preliminary findings reinforce the potential utility of approaches such as quantitative electroencephalography and motor cortical stimulation paradigms.\ud \ud SIGNIFICANCE: Various neurophysiological techniques have the potential to be useful biomarkers in the LBDs. We recommend that future studies focus on maximising the diagnostic specificity and sensitivity of the most promising neurophysiological biomarkers.

OBJECTIVE: The level of hippocampal atrophy in dementia with Lewy bodies (DLB) is typically less than that observed in Alzheimer's disease (AD). However, it is not known how the cognitive phenotype of DLB is influenced by hippocampal atrophy or the atrophy of adjacent medial temporal lobe structures. METHODS: Dementia with Lewy bodies (n = 65), AD (n = 76) and control (n = 63) participants underwent 3T magnetic resonance imaging and cognitive Cambridge Cognitive Examination and Mini-Mental State Examination (CAMCOG and MMSE) assessments. Hippocampal volume, and parahippocampal, entorhinal and temporal pole cortical thickness, was compared between groups. Regression models were used to investigate whether hippocampal volume and cortical thickness associated with global cognition and cognitive subdomains. RESULTS: Dementia with Lewy bodies, AD and control participants showed significantly different hippocampal, parahippocampal and entorhinal cortical thinning, where atrophy was greatest in AD and intermediate in DLB. Temporal pole thickness was reduced in DLB and AD compared with control participants. In DLB, but not AD, hippocampal volume associated with total CAMCOG, CAMCOG memory and MMSE scores. In DLB, parahippocampal, entorhinal and temporal pole thickness associated with total CAMCOG and CAMCOG memory scores, parahippocampal thickness associated with MMSE scores, and entorhinal thickness associated with CAMCOG executive function scores. CONCLUSIONS: In this large sample, these results are in agreement with other studies indicating that hippocampal atrophy is less severe in DLB than AD. Hippocampal atrophy and medial temporal lobe cortical thickness were associated with the severity of cognitive symptoms, suggesting that atrophy in these structures, as a potential proxy of AD pathology, may partly mediate specific DLB cognitive symptoms. © 2017 The Authors. International Journal of Geriatric Psychiatry Published by John Wiley & Sons Ltd.