Folia neuropathologica最新文献

Introduction: Postherpetic neuralgia (PHN) is one of the common refractory neuropathic pains. Oral drug treatment has great side effects and poor efficacy. To study the efficacy of computed tomography (CT)-guided pulsed radiofrequency (PRF) targeting dorsal root ganglion (DRG) and platelet-rich plasma (PRP), this retrospective observation was performed.

Material and methods: All patients with PHN were divided into the control group, PRF group, and PRF + PRP group based on their different treatment methods. The control group (45 cases) received drug treatment, the PRF group (45 cases) received CT-guided PRF treatment targeted to DRG, and the PRF + PRP group received PRF and PRP treatment. The changes of the numeric rating scale (NRS), Pittsburgh sleep quality index (PSQI) levels, and short form 36 health survey questionnaire (SF-36) before treatment and 7 days, 14 days, 30 days, and 90 days after treatment were compared among three groups.

Results: NRS and PSQI scores in the PRF + PRP group were lower than those in the PRF group and control group at 90 days after treatment ( p < 0.001). At 90 days after the operation, the scores of SF-36 in the PRF + PRP group were obviously elevated compared with the data of the control group and PRF group ( p < 0.001).

Conclusions: The pain degree, quality of sleep of patients, and quality of life with PHN were significantly improved after PRF combined with PRP treatments.

Introduction: Vasospasm has been reported as the most important cause of mortality and morbidity in patients with subarachnoid haemorrhage (SAH) who can reach the hospital. Matrix metalloproteinases (MMPs) are a gene family, which are called neutral proteases in the central nervous system (CNS). In this experimental study we studied the upregulation of MMPs (MMP-8, MMP-9, and MMP-13) gene expression and the inhibitor effects of doxycycline after experimental SAH model in rats.

Material and methods: After 24 Wistar Albino rats were divided into groups, a SAH model was created by transfusion of autologous blood from the cisterna magna, and then 30 mg/kg doxycycline treatment was applied. In order to observe the efficacy of the treatment, MMP-8, MMP-9 and MMP-13 gene expression levels were examined, and histopathological examinations were made in the sections taken.

Results: There was a statistically significant increase ( p < 0.05) in MMP-8, MMP-9 and MMP-13 gene expression within the first 6 hours after SAH. The Ct parameter specifies the number of cycles in which the detected fluorescence radiation threshold value is exceeded. The MMP-13 Ct difference in the SAH group was significantly higher ( p = 0.037) than the control group.

Conclusions: The pathophysiology of cerebral vasospasm is complex and multifactorial. Many studies are conducted to solve the complex mechanism of cerebral vasospasm. It has been shown that the use of doxycycline causes a statistically significant ( p < 0.05) inhibition at gene expression levels (MMP-8, MMP-9 and MMP-13), even in a single dose of usage and also these results have been confirmed by histopathology examination.

Cytidine-5'-diphosphocholine (CDP-choline) is a key precursor for the intracellular synthesis of phosphatidylcholine and other phospholipids. Following either intravenous or oral application citicoline (CDP-choline of exogenous origin) undergoes quick decomposition to cytidine and choline, and for this reason it is frequently considered a prodrug. However, upon acute intravenous application in mice citicoline is, on a molar basis, 20 times less toxic than choline. To find out whether cytidine may attenuate toxicity of choline, in the present experiments we compared maximum tolerated doses of single intravenous injections of choline and equimolar mixture of choline and cytidine. We assumed that, if after oral intake a substantial part of citicoline is catabolised already in the intestine and its catabolites enter blood separately, intravenously applied equimolar mixture of cytidine and choline will be markedly less toxic than an equivalent molar dose of choline. However, the maximum tolerated single doses determined in our experiment for choline and equimolar mixture of choline and cytidine were similar. These data suggest that citicoline taken orally is not significantly decomposed in the intestinal lumen, but absorbed to blood as the intact molecule.

The neuroinflammation is a crucial component of virtually all neurodegenerative disorders, including Alzheimer's disease (AD). The bacterial lipopolysaccharide (LPS), a potent activator of the innate immune system, was suggested to influence or even trigger the neuropathological alterations in AD. LPS-induced neuroinflammation involves changes in transcription of several genes, thus controlling these molecular processes may be a potentially efficient strategy to attenuate the progression of AD. Since genome-wide association studies showed that the majority of AD-related genetic risk factors (AD-GRF) are connected to the immune system, our aim was to identify AD-GRF affected in the hippocampus by LPS-induced systemic inflammatory response (SIR). Moreover, we analysed the role of bromodomain and extraterminal domain (BET) proteins, the readers of the acetylation code, in controlling the transcription of selected AD-GRF in the brain during neuroinflammation. In our study, we used a mouse model of LPS-induced SIR and mouse microglial BV2 cells. JQ1 was used as an inhibitor of BET proteins. The level of mRNA was analysed using microarrays and qPCR. Our data demonstrated that among the established AD-GRF, only the expression of Cd33 was significantly upregulated in the hippocampus during SIR. In parallel, we observed an increase in the expression of Brd4, a BET family member. JQ1 prevented an LPS-evoked increase in Cd33 expression in the hippocampus of mice. Moreover, JQ1 reduced Cd33 expression in BV2 microglial cells stimulated with blood serum from LPS-treated mice. Our study suggests that LPS-evoked SIR may increase Cd33 gene expression in the brain, and inhibition of BET proteins through suppression of Cd33 expression could be a promising strategy in prevention or in slowing down the progression of neuroinflammation and may potentially affect the pathomechanism of AD.