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Copenhagen, Denmark

Boutin H.,University of Manchester | Pinborg L.H.,Neurobiology Research Unit
Clinical and Translational Imaging | Year: 2015

Stroke is a major health problem in developed countries and neuroinflammation has emerged over the last 2 decades as major contributor to the pathophysiological processes of brain damage following stroke. PET imaging of the translocator 18 kDa protein (TSPO) provides a unique non-invasive point of access to neuroinflammatory processes and more specifically microglial and astrocytic reaction after stroke in both animal models and patients. Here, we are reviewing both the experimental and clinical literature about in vivo TSPO PET and SPECT imaging in stroke. The studies in animal models of stroke reviewed here highlight a slightly faster time-course for TSPO expression in permanent vs. temporary stroke and a stronger activation in the infarct core in temporary stroke vs. a stronger activation in peri-infarct areas in permanent stroke. Altogether these findings suggest that areas where neuroinflammatory events occur post-stroke are at higher risk of secondary damage. The time-course of TSPO expression is slower in humans versus animal models of stroke. In human studies, the TSPO expression in the peri-infarct areas peaks 3–4 weeks after stroke and increased TSPO expression is demonstrated for months after the stroke in remote areas both ipsilesional to pyramidal tracts damage and in the contralesional hemisphere. Further clinical studies are warranted to address the role of TSPO and neuroinflammation in functional recovery and reorganization after stroke and the possible therapeutic implications. TSPO imaging appears to be a valid biomarker for demonstrating the dynamic process of neuroinflammation in stroke. But it is also clear that as the processes of microglial activation are increasingly complex, the need for new biomarkers and tracers targeting other aspect of glial reaction are needed to further investigate neuroinflammatory processes in patients. © 2015, Italian Association of Nuclear Medicine and Molecular Imaging. Source


Pyndt Jorgensen B.,Copenhagen University | Hansen J.T.,Copenhagen University | Krych L.,Copenhagen University | Larsen C.,Copenhagen University | And 5 more authors.
PloS one | Year: 2014

Major depressive disorder is a debilitating disease in the Western World. A western diet high in saturated fat and refined sugar seems to play an important part in disease development. Therefore, this study is aimed at investigating whether saturated fat or sucrose predisposes mice to develop behavioral symptoms which can be interpreted as depression-like, and the possible influence of the gut microbiota (GM) in this. Fourty-two mice were randomly assigned to one of three experimental diets, a high-fat, a high-sucrose or a control diet for thirteen weeks. Mice on high-fat diet gained more weight (p = 0.00009), displayed significantly less burrowing behavior than the control mice (p = 0.034), and showed decreased memory in the Morris water maze test compared to mice on high-sucrose diet (p = 0.031). Mice on high-sucrose diet burrowed less goal-oriented, showed greater latency to first bout of immobility in the forced swim test when compared to control mice (p = 0.039) and high-fat fed mice (p = 0.013), and displayed less anxiety than mice on high-fat diet in the triple test (p = 0.009). Behavioral changes were accompanied by a significant change in GM composition of mice fed a high-fat diet, while no difference between diet groups was observed for sucrose preferences, LPS, cholesterol, HbA1c, BDNF and the cytokines IL-1α, IL-1β, IL-6, IL-10, IL-12(p70), IL-17 and TNF-α. A series of correlations was found between GM, behavior, BDNF and inflammatory mediators. In conclusion, the study shows that dietary fat and sucrose affect behavior, sometimes in opposite directions, and suggests a possible association between GM and behavior. Source


Vinberg M.,Copenhagen University | Froekjaer V.G.,Neurobiology Research Unit | Kessing L.V.,Copenhagen University
Journal of Nervous and Mental Disease | Year: 2010

Coping styles may influence the perceived life stress experienced by an individual and, therefore, also be critical in the development of affective disorders. This study examined whether familial risk of affective disorder is associated with the use of maladaptive coping styles, in healthy individuals. One hundred twelve high-risk and 78 low-risk individuals were identified through nation-wide registers and invited to participate in an extensive psychiatric evaluation including the Coping Inventory for Stressful Situations. The high-risk individuals used more Emotion-oriented (p = 0.001) and Avoidance coping (p = 0.04) than individuals not at risk. Adjusted for gender, age, years of education, and recent stressful life events the high-risk individuals used more emotion-oriented coping (p = 0.03). In conclusion, maladaptive coping style may represent a trait marker for mood disorder improving maladaptive coping styles may be a target for selective prevention focusing on subgroups at high risk of developing an affective disorder. © 2010 by Lippincott Williams & Wilkins. Source


Frederiksen K.S.,Danish Dementia Research Center | Sobol N.,Musculoskeletal Rehabilitation Research Unit | Sobol N.,Institute of Sports Medicine | Beyer N.,Musculoskeletal Rehabilitation Research Unit | And 4 more authors.
International Journal of Geriatric Psychiatry | Year: 2014

Objectives: Physical exercise may modulate neuropathology and symptoms of Alzheimer's disease (AD). This pilot study assessed the feasibility of conducting a study of moderate-to-high intensity aerobic exercise in home-dwelling patients with mild AD. Methods: An uncontrolled preintervention-postintervention test design with a single group receiving the same intervention. A total of eight patients with mild to moderate AD from the Copenhagen Memory clinic were included in the study. The intervention lasted for 14 weeks and consisted of supervised, 1-h sessions of aerobic exercise three times per week (50-60% of heart rate reserve for a two-week adaptation period and 70-80% of heart rate reserve for the remaining 12 weeks) Feasibility was assessed based on acceptability, including attendance and drop-out, safety, and patients' and caregivers' attitudes towards the intervention as well as other relevant parameters. Results: Attendance (mean, range: 90%, 70-100%) and retention (seven out of eight) rates were very high. No serious adverse events were observed. In general, patients and caregivers were positive towards the intervention. Conclusion: This study shows that it is feasible to conduct moderate-to-high intensity aerobic exercise in community-dwelling patients with mild AD. Our findings indicate that aspects such as a longer adaptation period, information about injury prevention, and need for involvement and support from caregivers should be addressed when planning an exercise intervention in an AD population. Copyright © 2014 John Wiley & Sons, Ltd. Source


Marner L.,Neurobiology Research Unit | Marner L.,Center for Integrated Molecular Brain Imaging | Frokjaer V.G.,Neurobiology Research Unit | Frokjaer V.G.,Center for Integrated Molecular Brain Imaging | And 12 more authors.
Neurobiology of Aging | Year: 2012

In patients with Alzheimer's disease (AD), postmortem and imaging studies have revealed early and prominent reductions in cerebral serotonin 2A (5-HT 2A) receptors. To establish if this was due to a selective disease process of the serotonin system, we investigated the cerebral 5-HT 2A receptor and the serotonin transporter binding, the latter as a measure of serotonergic projections and neurons. Twelve patients with AD (average Mini Mental State Examination [MMSE]: 24) and 11 healthy age-matched subjects underwent positron emission tomography (PET) scanning with [ 18F]altanserin and [ 11C]N,N-Dimethyl-2-(2-amino-4-cyanopheylthio)benzylamine ([ 11C]DASB). Overall [ 18F]altanserin binding was markedly reduced in AD by 28%-39% (p = 0.02), whereas the reductions in [ 11C]DASB binding were less prominent and mostly insignificant, except for a marked reduction of 33% in mesial temporal cortex (p = .0005). No change in [ 11C]DASB binding was found in the midbrain. We conclude that the prominent reduction in neocortical 5-HT 2A receptor binding in early AD is not caused by a primary loss of serotonergic neurons or their projections. © 2012 Elsevier Inc.. Source

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