Procalcitonin (PCT) is an established marker for severe systemic bacterial infection and sepsis in blood. Here we measured PCT by immunoassay in CSF and matched serum/plasma samples of controls and patients with different primary dementia disorders and acute neuroinflammation. PCT in CSF was significantly increased in patients with probable Alzheimer's disease, vascular dementia, dementia with Lewy bodies, frontotemporal dementia and acute neuroinflammation (encephalitis, meningitis) compared to non-demented controls. In contrast, PCT levels in matched plasma samples were normal in dementia groups, but elevated in meningitis/encephalitis. Our results indicate a central production of PCT and suggest PCT as a valuable marker candidate for the monitoring of dementia and acute neuroinflammation.
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"There is increasing evidence that inflammation and neurodegeneration are related events. Procalcitonin increases in cerebrospinal fluid (CSF) of AD, vascular dementia, dementia with Lewy bodies and frontotemporal dementia patients as well as acute neuroinflammatory states . To date, long-term consequences of septic encephalopathy are poorly understood. "
[Show abstract][Hide abstract]ABSTRACT: Survivors from sepsis present long-term cognitive deficits and some of these alterations resemble the pathophysiological mechanisms of neurodegenerative diseases. For this reason, we analyzed beta-amyloid peptide (Aβ) and synaptophysin levels in the brain of rats that survived from sepsis and their relation to cognitive dysfunction and to acute brain inflammation. Sepsis was induced in rats by cecal ligation and puncture, and 30 days after surgery, the hippocampus and prefrontal cortex were isolated just after cognitive evaluation by the inhibitory avoidance test. The immunocontent of Aβ and synaptophysin were analyzed by Western blot analysis. Aβ increased and synaptophysin decreased in septic animals both in the hippocampus and prefrontal cortex concurrent with the presence of cognitive deficits. Prefrontal levels of synaptophysin correlated to the performance in the inhibitory avoidance. Two different treatments known to decrease brain inflammation and oxidative stress when administered at the acute phase of sepsis decreased Aβ levels both in the prefrontal cortex and hippocampus, increased synaptophysin levels only in the prefrontal cortex, and improved cognitive deficit in sepsis-survivor animals. In conclusion, we demonstrated that brain from sepsis-survivor animals presented an increase in Aβ content and a decrease in synaptophysin levels and cognitive impairment. These alterations can be prevented by treatments aimed to decrease acute brain inflammation and oxidative stress.
Full-text · Article · Aug 2013 · Molecular Neurobiology
[Show abstract][Hide abstract]ABSTRACT: This chapter discusses the influence of coal type, pyrolysis conditions, demineralization, and iron catalyst on the formation of nitrogen (N2) during the fix-bed pyrolysis of several coals with different ranks. The analyses of five coals with size fraction 150–250 μm, where the nitrogen contents are around 2 % are tabulated in the chapter. Two coals, ZN and NS coal are demineralized at elevated temperatures with hydrochloric acid and sodium hydroxide, respectively. The high-temperature ashes from the original and demineralized coals are characterized by X-ray diffraction (XRD) analysis. Nitrogen conversions to N2 and char nitrogen in the fixed-bed pyrolysis of coals at 1000° C are strongly dependent on the coal type, and at the highest, 50 % of coal nitrogen is converted to N2. Conversion to N2 increases linearly with increasing pyrolysis temperature in the range of 600–1000° C, but contrarily, nitrogen retention in the char decreases with temperature. When a low-rank coal containing large amounts of exchangeable metal cations is demineralized by acid washing, conversion to N2 decreases drastically. A nanophase iron catalyst promotes the formation of N2.
[Show abstract][Hide abstract]ABSTRACT: Midregional Proenkephalin A (MR-PENK A) and N-terminal Protachykinin A (NT-PTA) are stable fragments of the precursor peptides for enkephalins and substance P, respectively. We measured MR-PENK A and NT-PTA concentrations by sensitive chemiluminescence immunoassays in cerebrospinal fluid (CSF) of 19 neurologically healthy controls (NHC), 28 patients with other neurologic disorders (OND), 70 patients with dementia disorders (38 Alzheimer's disease [AD], 8 dementia with Lewy bodies [DLB], 12 frontotemporal dementia [FTD], and 12 patients with vascular dementia [VD]), and 16 patients with acute neuroinflammation (AN). Median concentrations of NT-PTA were decreased in all patient groups compared to NHC showing significant differences between patients with NHC and AN (p<0.001), OND and AN (p<0.001), FTD and AN (p<0.01) and pAD and AN (p<0.05). Median MR-PENK A levels were lower in patients with OND, dementia disorders (including AD, FTD, DLB and VD) and AN compared to NHC subjects, although this differences did not reach statistical significance (p>0.05). A maximum difference of both proneuropeptide fragments was found between NHC subjects and patients with AN, with a more than 2fold decrease in median NT-PTA and a 1.5fold decrease in median MR-PENK A levels. Concentrations of both proneuropeptide fragments were positively correlated in all patients (r=0.77, p<0.001). Our results indicate alterations of the cerebral PENK A- and PTA-system in both, dementia and acute neuroinflammatory disorders. These neuropeptide systems seem to be highly correlated in healthy and pathological status.
No preview · Article · Mar 2010 · Journal of neuroimmunology