Proteomic analysis of cerebrospinal fluid from patients with idiopathic temporal lobe epilepsy

Xiao, Fei; Chen, Dan; Lü, Yang; Xiao, Zheng; Guan, Li-feng; Yuan, Jie; Wang, Liang; Xi, Zhiqin; Wang, Xuefeng

doi:10.1016/j.brainres.2008.12.008

Cited by 66 publications

(53 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similar up-regulations of this multifunctional protein, which acts as a transporter of vitamin D sterols and fatty acids, by activating macrophage and chemotaxis, and as a scavenger [12], have been reported in many other neurological diseases [23,21,3,32]. Therefore, it is likely that vitamin D-binding protein up-regulation in CSF could represent a non-specific reaction to neurological inflammatory, or even non-inflammatory insults, with possible beneficial functions on post-inflammatory tissue repair.…”

supporting

confidence: 56%

“…Some proteins, such as transthyretin, apolipoprotein A-IV, vitamin D-binding protein, and haptoglobin, which were differentially regulated in the CSF of our GBS patients vs. controls, have been reported to be expressed in the CSF of patients with very different diseases, which range from neuromyelitis optica, a severe inflammatory CNS disease (transthyretin and vitamin D-binding protein [3]), and viral meningitis or multiple sclerosis (vitamin Dbinding protein [21]), to non-overtly-inflammatory CNS diseases, such as temporal lobe epilepsy (vitamin D-binding protein [32]), lumbar disk herniation (apolipoprotein A-IV and vitamin D-binding protein [23]), Alzheimer disease (transthyretin [26,11]), and amyotrophic lateral sclerosis (transthyretin [25]). As a result, it is likely that the relative-to-total-protein CSF concentration of these proteins is non-specifically influenced by very different neurological pathologies, and therefore it is very unlikely that they can be used as biomarkers in GBS.…”

mentioning

confidence: 91%

See 1 more Smart Citation

Protein profiling of Guillain–Barrè syndrome cerebrospinal fluid by two-dimensional electrophoresis and mass spectrometry

D’Aguanno

Franciotta

Lupisella

et al. 2010

Neuroscience Letters

View full text Add to dashboard Cite

a b s t r a c tProtein profiling of cerebrospinal fluid in Guillain-Barrè syndrome (GBS), an acute and immune-mediated disease affecting the peripheral nervous system, was performed by two-dimensional electrophoresis. Significant modulated spots in GBS patients vs. control groups (a group of multiple sclerosis patients and one of healthy donors) underwent MALDI-TOF/TOF investigation. Inflammation-related proteins, such as vitamin D-binding protein, beta-2 glycoprotein I (ApoH), and a complement component C3 isoform were up-regulated in GBS, whereas transthyretin (the monomer and the dimer forms), apolipoprotein E, albumin and five of its fragments were down-regulated. Then, we used an isoelectric-focusingdinitrophenylhydrazine-based technique to analyse the extent of carbonylation and, as a result, of oxidative damage of GBS CSF proteome. We observed a major sensitivity to carbonylation for albumin and alpha-glycoprotein in inflammation and a selective increase of reactivity for a glycosylated Fab from an IgM globulin in GBS CSF. Our results add new proteins to candidate CSF features of GBS, and suggest that oxidative stress could contribute to the immunopathological mechanisms in this syndrome.

show abstract

supporting

confidence: 56%

mentioning

confidence: 91%

Protein profiling of Guillain–Barrè syndrome cerebrospinal fluid by two-dimensional electrophoresis and mass spectrometry

D’Aguanno

Franciotta

Lupisella

et al. 2010

Neuroscience Letters

View full text Add to dashboard Cite

show abstract

“…This hypothetical neurodegenerative role of DBP agrees with the higher CSF DBP concentrations found in SPMS, in which neurodegeneration becomes the main pathological feature. Remarkably, further support for this association between DBP and neuronal dysfunction comes from the identification of increased DBP levels in the CSF in other neurological disorders such as epilepsy, Alzheimer, and Parkinson disease [47,50]. These findings suggest that DBP could either play an active neurodegenerative function or merely be a marker of damaged neuronal tissue.…”

Section: Explanationsmentioning

confidence: 86%

The emerging role of vitamin D binding protein in multiple sclerosis

et al. 2010

View full text Add to dashboard Cite

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS). A growing body of evidence supports a role for vitamin D in MS aetiology. Vitamin D binding protein (DBP) is the major plasma carrier of vitamin D metabolites and genetic differences in DBP gene have been found to influence vitamin D levels. We review here evidence supporting a role of DBP in MS. Several recent studies show that DBP levels in the cerebrospinal fluid correlate with MS course, being lower during relapses and higher in the secondary progressive phase. Further studies are needed to elucidate the potential use of DBP as a biological marker of MS course, but may be of use given the current lack of diagnostic tools for the prediction of MS development and progression.

show abstract

“…However, the function of ILEI in the nervous system remains largely unknown, except for its possible role in development of the Xenopus retina 38 is associated with an increased risk of AD 40 , and the neuronal expression of TGF-b type II receptors is reduced in AD brains from the early stage of disease development 31 . In addition, recent proteomic analysis of cerebrospinal fluid revealed significantly decreased ILEI levels in patients with idiopathic temporal lobe epilepsy 41 , in whom the age-related incidence of Ab plaques in temporal cortex is significantly higher compared with agematched controls 42 . The ILEI level in cerebrospinal fluid may also be a biomarker for AD 43 .…”

Section: Discussionmentioning

confidence: 99%

The FAM3 superfamily member ILEI ameliorates Alzheimer’s disease-like pathology by destabilizing the penultimate amyloid-β precursor

et al. 2014

View full text Add to dashboard Cite

Accumulation of amyloid-b peptide (Ab) in the brain underlies the pathogenesis of Alzheimer's disease (AD). Ab is produced by b-and g-secretase-mediated sequential proteolysis of amyloid-b precursor protein (APP). Here we identify a secretory protein named interleukinlike epithelial-mesenchymal transition inducer (ILEI, also known as FAM3 superfamily member C) as a negative regulator of Ab production. ILEI destabilizes the b-secretasecleaved APP carboxy-terminal fragment, the penultimate precursor of Ab, by binding to the g-secretase complex and interfering with its chaperone properties. Notch signalling and g-secretase activity are not affected by ILEI. We also show neuronal expression of ILEI and its induction by transforming growth factor-b signalling. The level of secreted ILEI is markedly decreased in the brains of AD patients. Transgenic (Tg) overexpression of ILEI significantly reduces the brain Ab burden and ameliorates the memory deficit in AD model mice. ILEI may be a plausible target for the development of disease-modifying therapies.

show abstract

Proteomic analysis of cerebrospinal fluid from patients with idiopathic temporal lobe epilepsy

Cited by 66 publications

References 42 publications

Protein profiling of Guillain–Barrè syndrome cerebrospinal fluid by two-dimensional electrophoresis and mass spectrometry

Protein profiling of Guillain–Barrè syndrome cerebrospinal fluid by two-dimensional electrophoresis and mass spectrometry

The emerging role of vitamin D binding protein in multiple sclerosis

The FAM3 superfamily member ILEI ameliorates Alzheimer’s disease-like pathology by destabilizing the penultimate amyloid-β precursor

Contact Info

Product

Resources

About