|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
BEFREE |
At the blood-brain barrier, claudin-5 is the most enriched tight junction protein and its dysfunction has been implicated in neurodegenerative disorders such as Alzheimer's disease, neuroinflammatory disorders such as multiple sclerosis as well as psychiatric disorders including depression and schizophrenia.
|
30691500 |
2019 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
BEFREE |
However, although there is no common mechanism underpinning BBB dysfunction even within each particular disorder, the tight junction protein claudin-5 may be a clinically relevant target given that both clinical and pre-clinical research has linked it to schizophrenia, ASD, and depression.
|
29966749 |
2018 |
|
Schizophrenia
|
0.390 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that a variant in the claudin-5 gene is weakly associated with schizophrenia in 22q11DS, leading to 75% less claudin-5 being expressed in endothelial cells.
|
28993710 |
2018 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
BEFREE |
Here, we focus on the endothelial tight-junction protein claudin-5 (CLDN5), because the <i>CLDN5</i> gene is mapped to the schizophrenia-associated 22q11.2 deletion region, and a single nucleotide polymorphism in the <i>CLDN5</i> locus is also linked to schizophrenia.
|
29212157 |
2017 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
BEFREE |
CLDN-5 protein was increased in ASD cortex and cerebellum, while CLDN-12 appeared reduced in both ASD and SCZ cortexes.
|
27957319 |
2016 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
LHGDN |
Further study of a genetic association between the CLDN5 locus and schizophrenia.
|
15820333 |
2005 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
PSYGENET |
The present results suggest that the PLA2G4A locus may be involved in schizophrenia and its combination with the CLDN5 gene may increase further the risk for the illness.
|
16181776 |
2005 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
LHGDN |
Gene, gut and schizophrenia: the meeting point for the gene-environment interaction in developing schizophrenia.
|
15617864 |
2005 |
|
Schizophrenia
|
0.390 |
GeneticVariation
|
disease |
BEFREE |
The present results suggest that the PLA2G4A locus may be involved in schizophrenia and its combination with the CLDN5 gene may increase further the risk for the illness.
|
16181776 |
2005 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
LHGDN |
Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.
|
15363474 |
2004 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
PSYGENET |
Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.
|
15363474 |
2004 |
|
Schizophrenia
|
0.390 |
Biomarker
|
disease |
BEFREE |
Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.
|
15363474 |
2004 |
|
Respiratory Hypersensitivity
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Claudins, VEGF, Nrf2, Keap1, and Nonspecific Airway Hyper-Reactivity Are Increased in Mice Co-Exposed to Allergen and Acrolein.
|
30608172 |
2019 |
|
Infarction, Middle Cerebral Artery
|
0.200 |
Therapeutic
|
disease |
RGD |
Protective effect of naringenin in experimental ischemic stroke: down-regulated NOD2, RIP2, NF-κB, MMP-9 and up-regulated claudin-5 expression.
|
24842554 |
2014 |
|
Alzheimer's Disease
|
0.050 |
Biomarker
|
disease |
BEFREE |
At the blood-brain barrier, claudin-5 is the most enriched tight junction protein and its dysfunction has been implicated in neurodegenerative disorders such as Alzheimer's disease, neuroinflammatory disorders such as multiple sclerosis as well as psychiatric disorders including depression and schizophrenia.
|
30691500 |
2019 |
|
Alzheimer's Disease
|
0.050 |
Biomarker
|
disease |
BEFREE |
The analysis of the mechanism demonstrated that reduction of LINC00094 inhibited Endophilin-1 expression by up-regulating miR-224-4p/miR-497-5p, promoted the expression of ZO-1, occludin and claudin-5, and ultimately alleviated BBB permeability in AD microenvironment.
|
30801976 |
2019 |
|
Alzheimer's Disease
|
0.050 |
Biomarker
|
disease |
BEFREE |
By quantifying the amounts of major tight junction proteins, claudin-5 and occludin, in 12 brain regions dissected from post-mortem brains of normal ageing (n = 10), pathological ageing (n = 14) and Alzheimer's disease patients (n = 19), we found that they were selectively decreased in cortical areas in Alzheimer's disease.
|
30770921 |
2019 |
|
Alzheimer's Disease
|
0.050 |
Biomarker
|
disease |
BEFREE |
We investigated the effects of CAA on BBB integrity by examining the expression of the endothelial marker CD31, basement membrane protein collagen IV (COL4), tight junction protein claudin-5, and fibrinogen, a marker of BBB leakage, by immunohistochemistry in the occipital cortex of autopsy brains with AD and capillary CAA (CAA type 1; n = 8), AD with noncapillary CAA (CAA type 2; n = 10), and AD without CAA (n = 7) compared with elderly controls (n = 10).
|
30007166 |
2018 |
|
Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
We concluded that combined modulation of Wnt/Dkk-3/claudin-5 and TLR-4 pathways, simultaneously targeting apoptosis and survival signaling defects, might shift the balance from tumor growth stasis to cytotoxic therapeutic responses, flowing in greater therapeutic benefits.
|
30680070 |
2018 |
|
Cerebrovascular accident
|
0.050 |
Biomarker
|
group |
BEFREE |
Increased cerebral expressions of MMPs, CLDN5, OCLN, ZO1 and AQPs are associated with brain edema following fatal heat stroke.
|
28490769 |
2017 |
|
Cerebrovascular accident
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Rather, we demonstrate that α5 KOs have increased blood-brain barrier integrity (increased expression of claudin-5, and absent brain parenchymal IgG extravasation) after stroke compared with controls, which could explain their resistance to ischemic injury.
|
26661237 |
2017 |
|
Cerebrovascular accident
|
0.050 |
Biomarker
|
group |
BEFREE |
Patients with AIS were assigned to oxygen therapy or room air for 4 hours, and blood occludin and claudin-5 were measured at different time points after stroke.
|
28931617 |
2017 |
|
Cerebrovascular accident
|
0.050 |
AlteredExpression
|
group |
BEFREE |
PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice (p < 0.05), while MLA had the opposite effect.
|
27914011 |
2017 |
|
Alzheimer's Disease
|
0.050 |
Biomarker
|
disease |
BEFREE |
Our data corroborates the hypothesis that increased BCSFB permeability, especially loss of selective CLDN5-mediated paracellular transport, altered CSF production and CPE sink action, as well as loss of CPE mediated macrophage recruitment contribute to the pathogenesis of AD.
|
26573292 |
2015 |
|
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Quantitative analysis of the transcript and protein expression data showed that CLDN1 and CLDN5 were significantly down regulated (p=<0.001) in tumors of all four grades and model cell lines.
|
25345514 |
2014 |