Some markers of neuronal damage in cerebrospinal fluid of multiple sclerosis patients in relapse.

In this paper the performance of cerebrospinal fluid (CSF) protein biomarkers important for monitoring damage of brain astrocytes and neurons for MS is reviewed. We estimated neurofilament, tau and phospho-tau proteins, β-APP, Aβ, S-100B and neuron-specific enolase in CSF of MS patients during relapse. We noted elevation of neurofilament, tau and phospho-tau proteins, S-100B, neuron-specific enolase and c-terminal epitopes of β-APP; concomitantly decrease of Aβ was observed.

Free radical peroxidation products in cerebrospinal fluid and serum of patients with multiple sclerosis after glucocorticoid therapy.

Multiple sclerosis (MS) patients were found to have elevated thiobarbituric acid reactive material levels, increased soluble sulfhydryl groups and reduced protein sulfhydryl groups in cerebrospinal fluid and serum, and slightly reduced superoxide dismutase in serum, which suggested disease activating free radical peroxidation. Moreover, levels of these varied across methylprednisolone (MP) therapy. We observed significant differences in the levels of peroxidation products between MS patients and controls.

Homocysteine-induced acute excitotoxicity in cerebellar granule cells in vitro is accompanied by PP2A-mediated dephosphorylation of tau.

Our results demonstrate that acute exposure of primary rat cerebellar granule cell cultures to homocysteine at millimolar concentrations induces a glutamate receptor-mediated decrease in tau protein phosphorylation, which is accompanied by excitotoxic neuronal damage. This contrasts with the previously reported hyperphosphorylation of tau in homocysteine-treated neurons, and with the assumption that hyperhomocysteinemia is one of the risk factors in Alzheimer disease, in which abnormal hyperphosphorylation of tau protein leads to neurofibrillary degeneration. The mechanisms of homocysteine neurotoxicity have been explained mainly either by disturbances in methylation processes, that may also lead to the accumulation of phosphorylated tau due to reduced activity of tau-selective protein phosphatase 2A, or by excitotoxicity.

The immature endothelial cell in new vessel formation following surgical injury in rat brain.

Objectives: We investigated neovasculatization in the cerebral cortex of the adult rat after surgical brain injury by ultrastructural, immunocytochemical and immunochemical means. Previously we described endothelial-like cell that participates in new vessel formation on plasma proteins that served as a provisional matrix in the region immediately adjacent to the traumatic injury. In the present study we describe new vessel formation in the multistep process with the alterations in endothelial-like cell immunophenotype.

2-deoxyglucose induces beta-APP overexpression, tau hyperphosphorylation and expansion of the trans-part of the Golgi complex in rat cerebral cortex.

The effects of a single intraperitoneal injection of a non-metabolizable glucose analog 2-deoxyglucose (2-DG, 500 mg/kg) on the levels of beta-APP expression, and phosphorylated and unphosphorylated tau protein in the rat cerebral cortex were investigated. The effects of 2-DG on the ultrastructure of cortical neurons with particular emphasis on the morphology of the Golgi apparatus, and on brain bioenergetics assessed by in vivo 31P-MRS technique were also evaluated. Seven and a half hours after injection of 2-deoxyglucose a significant increase in brain cortex beta-APP expression, increased tau phosphorylation, and a marked relative expansion of the trans- part of the Golgi intracellular secretory pathway in cortical neurons has been found.

Cerebrospinal fluid free-radical peroxidation products and cognitive functioning patterns differentiate varieties of normal pressure hydrocephalus.

The aims of the study were as follows: first, to verify the hypothesis that free radical peroxidation may be one of the factors implicated in pathophysiology of normal pressure hydrocephalus (NPH) and, second, to find out whether these biochemical characteristics together with neuropsychological cognitive deficits can differentiate between various types of NPH. This provides prognostic criteria for selection of patients for shunt surgery. Lipid peroxidation was measured in terms of thiobarbituric acid-reactive material (TBAR) and protein sulphydryl (SH) groups were measured as CSF content.

N-methyl-d-aspartate receptor-mediated processing of beta-amyloid precursor protein in rat hippocampal slices: in vitro--superfusion study.

Abnormal proteolytic degradation of the beta amyloid precursor protein (beta-APP) may result in accumulation of potentially neurotoxic beta amyloid (betaA). The role of various receptors in the regulation of beta-APP processing has been suggested. This study aimed to determine how NMDA receptors and Ca2+ ions regulate proteolysis of beta-APP in rat hippocampus in vitro.