Autor: |
Fruekilde SK; Center for Functionally Integrative Neuroscience (CFIN), Department of Clinical Medicine, 1006Aarhus University, Aarhus C, Denmark.; Sino-Danish Center for Education and Research (SDC), University of Chinese Academy of Sciences, Beijing, P.R. China., Bailey CJ; Center for Functionally Integrative Neuroscience (CFIN), Department of Clinical Medicine, 1006Aarhus University, Aarhus C, Denmark.; Sino-Danish Center for Education and Research (SDC), University of Chinese Academy of Sciences, Beijing, P.R. China., Lambertsen KL; Department of Neurobiology Research, Institute of Molecular Medicine, 6174University of Southern Denmark, Odense C, Denmark.; BRIDGE - Brain Research - Inter-Disciplinary Guided Excellence, Department of Clinical Research, 6174University of Southern Denmark, Odense C, Denmark.; Department of Neurology, Odense University Hospital, Odense C, Denmark., Clausen BH; Department of Neurobiology Research, Institute of Molecular Medicine, 6174University of Southern Denmark, Odense C, Denmark.; BRIDGE - Brain Research - Inter-Disciplinary Guided Excellence, Department of Clinical Research, 6174University of Southern Denmark, Odense C, Denmark., Carlsen J; Research Unit for Molecular Medicine (MMF), Department of Clinical Medicine, 1006Aarhus University, Aarhus N, Denmark., Xu NL; Sino-Danish Center for Education and Research (SDC), University of Chinese Academy of Sciences, Beijing, P.R. China.; Institute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, P.R. China., Drasbek KR; Center for Functionally Integrative Neuroscience (CFIN), Department of Clinical Medicine, 1006Aarhus University, Aarhus C, Denmark.; Sino-Danish Center for Education and Research (SDC), University of Chinese Academy of Sciences, Beijing, P.R. China., Gutiérrez-Jiménez E; Center for Functionally Integrative Neuroscience (CFIN), Department of Clinical Medicine, 1006Aarhus University, Aarhus C, Denmark. |
Abstrakt: |
Systemic inflammation affects cognitive functions and increases the risk of dementia. This phenomenon is thought to be mediated in part by cytokines that promote neuronal survival, but the continuous exposure to which may lead to neurodegeneration. The effects of systemic inflammation on cerebral blood vessels, and their provision of adequate oxygen to support critical brain parenchymal cell functions, remains unclear. Here, we demonstrate that neurovascular coupling is profoundly disturbed in lipopolysaccharide (LPS) induced systemic inflammation in awake mice. In the 24 hours following LPS injection, the hyperaemic response of pial vessels to functional activation was attenuated and delayed. Concurrently, under steady-state conditions, the capillary network displayed a significant increase in the number of capillaries with blocked blood flow, as well as increased duration of 'capillary stalls'-a phenomenon previously reported in animal models of stroke and Alzheimer's disease pathology. We speculate that vascular changes and impaired oxygen availability may affect brain functions following acute systemic inflammation and contribute to the long-term risk of neurodegenerative changes associated with chronic, systemic inflammation. |