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Journal articleByrne CS, Chambers ES, Alhabeeb H, et al., 2016,
Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods
, American Journal of Clinical Nutrition, Vol: 104, ISSN: 1938-3207BACKGROUND: Short-chain fatty acids (SCFAs), metabolites produced through the microbial fermentation of nondigestible dietary components, have key roles in energy homeostasis. Animal research suggests that colon-derived SCFAs modulate feeding behavior via central mechanisms. In humans, increased colonic production of the SCFA propionate acutely reduces energy intake. However, evidence of an effect of colonic propionate on the human brain or reward-based eating behavior is currently unavailable. OBJECTIVES: We investigated the effect of increased colonic propionate production on brain anticipatory reward responses during food picture evaluation. We hypothesized that elevated colonic propionate would reduce both reward responses and ad libitum energy intake via stimulation of anorexigenic gut hormone secretion. DESIGN: In a randomized crossover design, 20 healthy nonobese men completed a functional magnetic resonance imaging (fMRI) food picture evaluation task after consumption of control inulin or inulin-propionate ester, a unique dietary compound that selectively augments colonic propionate production. The blood oxygen level-dependent (BOLD) signal was measured in a priori brain regions involved in reward processing, including the caudate, nucleus accumbens, amygdala, anterior insula, and orbitofrontal cortex (n = 18 had analyzable fMRI data). RESULTS: Increasing colonic propionate production reduced BOLD signal during food picture evaluation in the caudate and nucleus accumbens. In the caudate, the reduction in BOLD signal was driven specifically by a lowering of the response to high-energy food. These central effects were partnered with a decrease in subjective appeal of high-energy food pictures and reduced energy intake during an ad libitum meal. These observations were not related to changes in blood peptide YY (PYY), glucagon-like peptide 1 (GLP-1), glucose, or insulin concentrations. CONCLUSION: Our results suggest that colonic propionate production may play
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Journal articleSu T, Wit FW, Caan MW, et al., 2016,
White matter hyperintensities in relation to cognition in HIV-infected men with sustained suppressed viral load on cART
, AIDS, Vol: 30, Pages: 2329-2339, ISSN: 1473-5571OBJECTIVES: The objective of this study was to assess whether HIV-infected patients on long-term successful combination antiretroviral therapy (cART) have more extensive white matter hyperintensities (WMH) of presumed vascular origin compared with uninfected controls and whether these intensities are associated with cognitive impairment. Furthermore, we explored potential determinants of increased WMH loadin long-term suppressed HIV infection. DESIGN: A cross-sectional comparison of WMH in an observational cohort. METHODS: Clinical, cognitive and magnetic resonance imagingdata were collected from 103middle-aged, aviremic HIV-infected menon cART and 70 HIV-uninfected, otherwise similar controls. In the MRI data, WMH load was quantified by automated approaches and qualitatively reviewed by an experienced neuroradiologist using the Fazekas scale. RESULTS: HIV-infected men hadan increased WMHload. Among HIV-infected patients, increased WMH load was independently associated witholder age, higher diastolic blood pressure and D-dimer levels,and longer time spent with a CD4 count below 500 cells/mm. HIV-associated cognitive deficits were associated with increased WMHload. CONCLUSIONS: WMHare more extensive and associated with cognitive deficitsin middle-aged,aviremic cART-treated HIV-infected men. The extent of WMH load wasassociated with both cardiovascular risk factors and past immune deficiency. Since cognitive impairment in these same patients is also associated with these risk factors, this may suggest that in the setting of HIV, WMH and cognitive deficits share a common etiology. This supports the importance of optimizing cardiovascular risk management, and early, effective treatment of HIVinfection.
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Conference paperWhittington A, Sharp D, Gunn R, 2016,
Spatiotemporal distribution of beta-amyloid in Alzheimer's Disease results from heterogeneous regional carrying capacities
, Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505- Author Web Link
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- Citations: 2
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Journal articleJamall O, Feeney C, Zaw-Linn J, et al., 2016,
Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury
, Clinical Endocrinology, Vol: 85, Pages: 636-644, ISSN: 1365-2265Objectives: Traumatic brain injury (TBI) is a major cause of long-term disability with variable recovery. Preclinicalstudies suggest that vitamin D status influences recovery after TBI. However, there is no publishedclinical data on links between vitamin D status and TBI outcomes. To determine the: (i) prevalence ofvitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors andTBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI.Design: Retrospective audit of patients seen between July 2009 and March 2015. Serum vitamin D (25-hydroxy-cholecalciferol) was categorised as deficient (<40nmol/L), insufficient (40-70nmol/L) or replete(>70nmol/L).Patients: 353 adults seen in tertiary hospital clinic (75.4% lighter-skinned, 74.8% male, age median 35.1y,range 26.6-48.3y), 0.3-56.5 months after TBI (74.5% moderate-severe).Measurements: Serum vitamin D concentrations; Addenbrooke’s Cognitive Examination (ACE-R), BeckDepression Inventory II (BDI-II), SF-36 Quality of Life, Pittsburgh Sleep Quality Index.Results: 46.5% of patients after TBI had vitamin D deficiency and 80.2% insufficiency/deficiency. Patientswith vitamin D deficiency had lower ACE-R scores than those vitamin D replete (mean effect size ± SEM 4.5± 2.1, P=0.034), and higher BDI-II scores than those vitamin D insufficient (4.5 ± 1.6, P=0.003), correcting forage, gender, time since TBI, TBI severity. There was no association between vitamin D status and markers ofTBI severity, sleep or quality of life.Conclusion: Vitamin D deficiency is common in patients after TBI and associated with impaired cognitivefunction and more severe depressive symptoms.
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Conference paperUnderwood J, Cole JH, Sharp D, et al., 2016,
Brain MRI changes associated with poorer cognitive function despite suppressive antiretroviral therapy
, 22nd Annual Conference of the British HIV Association (BHIVA), Publisher: Wiley, Pages: 6-6, ISSN: 1464-2662 -
Journal articleScott GPT, Ramlackhansingh A, Edison P, et al., 2016,
Amyloid pathology and axonal injury after brain trauma
, Neurology, Vol: 86, Pages: 821-828, ISSN: 0028-3878Objective: To image amyloid-β (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer’s disease.Methods: Patients 11 months to 17 years after moderate-severe TBI had 11C-Pittsburgh compound-B (PIB) PET, structural and diffusion MRI and neuropsychological examination. Healthy aged controls and AD patients had PET and structural MRI. Binding potential (BPND) images of 11C-PIB, which index Aβ plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy (FA), was estimated and correlated with 11C-PIB BPND.Results: 28 participants (9 TBI, 9 controls, 10 AD) were assessed. Increased 11C-PIB BPND was found in TBI versus controls in the posterior cingulate cortex (PCC) and cerebellum. Binding in the PCC increased with decreasing FA of associated white matter tracts, and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions, but increased in the cerebellum. Conclusions: Increased Aβ burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathological features of dementia, which may relate to axonal damage produced by the injury.
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Journal articleLorenz R, Hampshire A, Leech R, 2016,
Neuroadaptive Bayesian Optimization and Hypothesis Testing
, TRENDS IN COGNITIVE SCIENCES, Vol: 21, Pages: 155-167, ISSN: 1364-6613 -
Journal articleOdlaug BL, Hampshire A, Chamberlain SR, et al., 2016,
Abnormal brain activation in excoriation (skin-picking) disorder: evidence from an executive planning fMRI study.
, Br J Psychiatry, Vol: 208, Pages: 168-174BACKGROUND: Excoriation (skin-picking) disorder (SPD) is a relatively common psychiatric condition whose neurobiological basis is unknown. AIMS: To probe the function of fronto-striatal circuitry in SPD. METHOD: Eighteen participants with SPD and 15 matched healthy controls undertook an executive planning task (Tower of London) during functional magnetic resonance imaging (fMRI). Activation during planning was compared between groups using region of interest and whole-brain permutation cluster approaches. RESULTS: The SPD group exhibited significant functional underactivation in a cluster encompassing bilateral dorsal striatum (maximal in right caudate), bilateral anterior cingulate and right medial frontal regions. These abnormalities were, for the most part, outside the dorsal planning network typically activated by executive planning tasks. CONCLUSIONS: Abnormalities of neural regions involved in habit formation, action monitoring and inhibition appear involved in the pathophysiology of SPD. Implications exist for understanding the basis of excessive grooming and the relationship of SPD with putative obsessive-compulsive spectrum disorders.
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Journal articleSu T, Caan MWA, Wit FWNM, et al., 2016,
White matter structure alterations in HIV-1-infected men with sustained suppression of viraemia on treatment
, AIDS, Vol: 30, Pages: 311-322, ISSN: 0269-9370Objective: Cognitive impairment is highly prevalent in HIV-1-infected (HIV+) patients, despite adequate suppression of viral replication by combination antiretroviral therapy (cART). Cerebral white matter structure alterations are often associated with cognitive impairment and have commonly been reported in the natural course of HIV infection. However, the existence of these alterations in adequately treated HIV+ patients remains unknown, as well as its possible association with cognitive impairment.Design: We used diffusion tensor imaging (DTI) to investigate whether white matter structure alterations exist in HIV+ patients with sustained suppressed viral replication on cART, and if such alterations are related to HIV-associated cognitive deficits.Methods: We compared 100 aviraemic HIV+ men on cART with 70 HIV-uninfected, otherwise comparable men. Clinical and neuropsychological assessments were performed. From DTI data, white matter fractional anisotropy and mean diffusion were calculated. Subsequently, tract-based spatial statistics (TBSS) was performed, with and without masking out white matter lesions.Results: HIV+ patients showed diffuse white matter structure alterations as compared with HIV-uninfected controls, observed as widespread decreased fractional anisotropy and an increased mean diffusion. These white matter structure alterations were associated with the number of years spent with a CD4+ cell count below 500 cells/µl, but not with HIV-associated cognitive deficits.Conclusion: Cerebral white matter structure alterations are found in middle-aged HIV+ men with sustained suppression of viraemia on cART, and may result from periods with immune deficiency when viral toxicity and host-inflammatory responses were at their peak. These white matter structure alterations were not associated with the observed subtle HIV-associated cognitive deficits.
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Conference paperLorenz R, Monti RP, Hampshire A, et al., 2016,
Towards tailoring non-invasive brain stimulation using real-time fMRI and Bayesian optimization
, 6th International Workshop on Pattern Recognition in Neuroimaging (PRNI), Publisher: IEEE, Pages: 49-52, ISSN: 2330-9989- Cite
- Citations: 1
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