Systemic inflammation and neuronal hyperexcitability: Deciphering cellular neuropathology of sickness behaviour

Author(s):  
Si-Si Lin ◽  
Alexei Verkhratsky
2011 ◽  
Vol 39 (4) ◽  
pp. 945-953 ◽  
Author(s):  
Colm Cunningham

It is widely accepted that inflammation plays some role in the progression of chronic neurodegenerative diseases such as AD (Alzheimer's disease), but its precise role remains elusive. It has been known for many years that systemic inflammatory insults can signal to the brain to induce changes in CNS (central nervous system) function, typically grouped under the syndrome of sickness behaviour. These changes are mediated via systemic and CNS cytokine and prostaglandin synthesis. When patients with dementia suffer similar systemic inflammatory insults, delirium is a frequent consequence. This profound and acute exacerbation of cognitive dysfunction is associated with poor prognosis: accelerating cognitive decline and shortening time to permanent institutionalization and death. Therefore a better understanding of how delirium occurs during dementia and how these episodes impact on existing neurodegeneration are now important priorities. The current review summarizes the relationship between dementia, systemic inflammation and episodes of delirium and addresses the basic scientific approaches currently being pursued with respect to understanding acute cognitive dysfunction during aging and dementia. In addition, despite there being limited studies on this subject, it is becoming increasingly clear that infections and other systemic inflammatory conditions do increase the risk of AD and accelerate the progression of established dementia. These data suggest that systemic inflammation is a major contributor to the progression of dementia and constitutes an important clinical target.


2011 ◽  
Vol 39 (4) ◽  
pp. 898-901 ◽  
Author(s):  
Clive Holmes ◽  
Joe Butchart

A number of studies demonstrate disturbances of the central innate immune system in AD (Alzheimer's disease). In animal and human studies, there is evidence of close communication between systemic and central innate immune systems. Animal models of neurodegeneration show evidence of an exaggerated central innate immune response following systemic inflammation. Clinical studies of AD show evidence of increased cognitive decline and exaggerated sickness behaviour in response to systemic inflammation. Recognition of this communication pathway offers alternative explanations for a number of recognized risk factors in the development and progression of AD and highlights the potential of the manipulation of systemic innate immunity as a novel therapeutic approach.


Author(s):  
Mehdi Ellouze ◽  
Lola Vigouroux ◽  
Colas Tcherakian ◽  
Paul‐Louis Woerther ◽  
Aurélie Guguin ◽  
...  

2018 ◽  
Vol 17 (2) ◽  
pp. 24-28
Author(s):  
O. M. Polikutina ◽  
Y. S. Slepynina ◽  
E. D. Bazdyrev ◽  
V. N. Karetnikova ◽  
O. L. Barbarach

Aim. To evaluate the structural and functional changes in the lungs of ST elevation myocardial infarction (STEMI) patients with absence or presence of chronic obstructive lung disease (COPD), and the relation with myocardial dysfunction and systemic inflammation.Material and methods. Totally, 189 STEMI patients included: group 1 — STEMI with COPD of moderate and mild grade, 2 — STEMI with no lung pathology. Groups were comparable by clinical and anamnestic parameters. Assessment of lung function and blood collection were done at 10­12 day of STEMI. For comparison of the parameters representing structural and functional changes in the lungs and comparison of C­reactive protein (CRP), N­terminal pro­brain natriuretic peptide (NT­proBNP) concentration, a control group was formed with no pulmonary pathology, comparable by age and sex with the STEMI patients.Results. In COPD patients, higher values revealed of the parameters representing the part of residual volumes in pulmonary structure. Higher residual volume (RV) was found also in STEMI and no COPD comparing to controls, however the relation RV/TLC (total lung capacity) was not higher than normal range. In both groups there were lower values of diffusion lung capacity (DLCO) comparing to controls. The lowest DLCO found in COPD patients. Concentration of NT­proBNP (H=41,6; p<0,001) and CRP (H=38,6; p<0,001) in COPD was significantly higher in STEMI with no COPD patients than in controls. The negative correlations found for NT­proBNP and CRP with forced expiratory volume 1 sec, FEV/FVC1, DLCO, and positive — with the values of thoracic volume, RV/TLC.Conclusion. In STEMI patients the increase revealed of residual lung volumes. Mostly the level of residual volumes is high in STEMI and COPD patients. There are associations of NT­proBNP and CRP with structural and functional parameters of the lungs regardless of COPD.


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