Non-Steroidal Anti-Inflammatory Drugs and Cognitive Function: Are Prostaglandins at the Heart of Cognitive Impairment in Dementia and Delirium ?

Studies of non-steroidal anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis imply that inflammation is important in the development of Alzheimer’s disease (AD). However, these drugs have not alleviated the symptoms of AD in those who have already developed dementia. This suggests that the primary mediator targeted by these drugs, PGE2, is not actively suppressing memory function in AD. Amyloid-β oligomers appear to be important for the mild cognitive changes seen in AD transgenic mice, yet amyloid immunotherapy has also proven unsuccessful in clinical trials. Collectively, these findings indicate that NSAIDs may target a prodromal process in mice that has already passed in those diagnosed with AD, and that synaptic and neuronal loss are key determinants of cognitive dysfunction in AD. While the role of inflammation has not yet become clear, inflammatory processes definitely have a negative impact on cognitive function during episodes of delirium during dementia. Delirium is an acute and profound impairment of cognitive function frequently occurring in aged and demented patients exposed to systemic inflammatory insults, which is now recognised to contribute to long-term cognitive decline. Recent work in animal models is beginning to shed light on the interactions between systemic inflammation and CNS pathology in these acute exacerbations of dementia. This review will assess the role of prostaglandin synthesis in the memory impairments observed in dementia and delirium and will examine the relative contribution of amyloid, synaptic and neuronal loss. We will also discuss how understanding the role of inflammatory mediators in delirious episodes will have major implications for ameliorating the rate of decline in the demented population

The increase of carcinoembryonic antigen (CEA), high-sensitivity C-reactive protein, and neutrophil/lymphocyte ratio in Parkinson’s disease

The role of carcinoembryonic antigen (CEA) in Parkinson's disease (PD) has not been previously investigated. The aim of the present study was to evaluate the serum level of carcinoembryonic antigen, high-sensitivity C-reactive protein (hs-CRP), and Neutrophil/lymphocyte ratio (NLR) among patients with Parkinson's disease and to examine the relationship between these inflammatory markers. The cross-sectional design includes 51 patients with Parkinson's disease and 50 age- and sex-matched healthy controls. We investigated the differences in hs-CRP, CEA, and NLR levels between these two groups. CEA was significantly higher in PD patients relative to the control group (mean 2.40 +/- A 1.51 vs. 1.72 +/- A 0.87 (ng/mL), respectively; p = 0.015). Mean NLR was significantly higher in PD patients relative to the control group (mean 3.1 +/- A 1.3 vs. 2.1 +/- A 0.32, respectively; p < 0.001). Serum level of hs-CRP was higher in PD patients than in control group (mean 1.04 +/- A 0.62 and 0.54 +/- A 0.31, respectively; p < 0.01). Correlation analysis revealed significant correlation between hs-CRP, CEA, and Neutrophil/lymphocyte ratio (p < 0.05). This study demonstrates for the first time the association between CEA, hs-CRP, NLR, and PD. We found CEA, hs-CRP, and NLR levels to be significantly higher in the PD patients than in the normal controls.Dicle University DUBAPWe are grateful to Dicle University DUBAP for their sponsorship about English editing of this manuscript

Aquaporin 4: a player in cerebral edema and neuroinflammation

<p>Abstract</p> <p>Neuroinflammation is a common pathological event observed in many different brain diseases, frequently associated with blood brain barrier (BBB) dysfunction and followed by cerebral edema. Neuroinflammation is characterized with microglia activation and astrogliosis, which is a hypertrophy of the astrocytes. Astrocytes express aquaporin 4, the water channel protein, involved in water homeostasis and edema formation. Aside from its function in water homeostasis, recent studies started to show possible interrelations between aquaporin 4 and neuroinflammation. In this review the roles of aquaporin 4 in neuroinflammation associated with BBB disruption and cerebral edema will be discussed with recent studies in the field.</p