scholarly journals Elucidating the Complex Interactions between Stress and Epileptogenic Pathways

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Aaron R. Friedman ◽  
Luisa P. Cacheaux ◽  
Sebastian Ivens ◽  
Daniela Kaufer
Keyword(s):  
Experimental Data ◽  
Blood Brain Barrier ◽  
Inflammatory Cytokine ◽  
Stress Hormones ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Complex Interactions ◽  
Narrow Focus ◽  
Analytical Tools

Clinical and experimental data suggest that stress contributes to the pathology of epilepsy. We review mechanisms by which stress, primarily via stress hormones, may exacerbate epilepsy, focusing on the intersection between stress-induced pathways and the progression of pathological events that occur before, during, and after the onset of epileptogenesis. In addition to this temporal nuance, we discuss other complexities in stress-epilepsy interactions, including the role of blood-brain barrier dysfunction, neuron-glia interactions, and inflammatory/cytokine pathways that may be protective or damaging depending on context. We advocate the use of global analytical tools, such as microarray, in support of a shift away from a narrow focus on seizures and towards profiling the complex, early process of epileptogenesis, in which multiple pathways may interact to dictate the ultimate onset of chronic, recurring seizures.

Role of thrombin-PAR1-PKCθ/δ axis in brain pericytes in thrombin-induced MMP-9 production and blood–brain barrier dysfunction in vitro

Neuroscience ◽  
2017 ◽  
Vol 350 ◽  
pp. 146-157 ◽  
Author(s):  
Takashi Machida ◽  
Shinya Dohgu ◽  
Fuyuko Takata ◽  
Junichi Matsumoto ◽  
Ikuya Kimura ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Brain Pericytes

scholarly journals The Dual Role of Microglia in Blood-Brain Barrier Dysfunction after Stroke

2020 ◽  
Vol 18 (12) ◽  
pp. 1237-1249 ◽  
Author(s):  
Ruiqing Kang ◽  
Marcin Gamdzyk ◽  
Cameron Lenahan ◽  
Jiping Tang ◽  
Sheng Tan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Vital Role ◽  
Dual Role ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
M2 Microglia ◽  
The Brain

It is well-known that stroke is one of the leading causes of death and disability all over the world. After a stroke, the blood-brain barrier subsequently breaks down. The BBB consists of endothelial cells surrounded by astrocytes. Microglia, considered the long-living resident immune cells of the brain, play a vital role in BBB function. M1 microglia worsen BBB disruption, while M2 microglia assist in repairing BBB damage. Microglia can also directly interact with endothelial cells and affect BBB permeability. In this review, we are going to discuss the mechanisms responsible for the dual role of microglia in BBB dysfunction after stroke.

scholarly journals The Role of Brain Microvascular Endothelial Cell and Blood-Brain Barrier Dysfunction in Schizophrenia

2020 ◽  
Vol 6 (1-2) ◽  
pp. 30-46
Author(s):  
Sovannarath Pong ◽  
Rakesh Karmacharya ◽  
Marianna Sofman ◽  
Jeffrey R. Bishop ◽  
Paulo Lizano
Keyword(s):  
Blood Brain Barrier ◽  
Association Studies ◽  
Central Element ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Genome Wide Association Studies ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Microvascular Endothelial

Background: Despite decades of research, little clarity exists regarding pathogenic mechanisms related to schizophrenia. Investigations on the disease biology of schizophrenia have primarily focused on neuronal alterations. However, there is substantial evidence pointing to a significant role for the brain’s microvasculature in mediating neuroinflammation in schizophrenia. Summary: Brain microvascular endothelial cells (BMEC) are a central element of the microvasculature that forms the blood-brain barrier (BBB) and shields the brain against toxins and immune cells via paracellular, transcellular, transporter, and extracellular matrix proteins. While evidence for BBB dysfunction exists in brain disorders, including schizophrenia, it is not known if BMEC themselves are functionally compromised and lead to BBB dysfunction. Key Messages: Genome-wide association studies, postmortem investigations, and gene expression analyses have provided some insights into the role of the BBB in schizophrenia pathophysiology. However, there is a significant gap in our understanding of the role that BMEC play in BBB dysfunction. Recent advances differentiating human BMEC from induced pluripotent stem cells (iPSC) provide new avenues to examine the role of BMEC in BBB dysfunction in schizophrenia.

1958-P: Role of Leptin in Blood-Brain Barrier Dysfunction

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1958-P
Author(s):  
THERESE S. SALAMEH ◽  
WILLIAM MORTELL ◽  
WILLIAM A. BANKS
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain

Role of Histaminergic System in Blood–Brain Barrier Dysfunction Associated with Neurological Disorders

2014 ◽  
Vol 45 (8) ◽  
pp. 677-686 ◽  
Author(s):  
Ivette Bañuelos-Cabrera ◽  
María Guadalupe Valle-Dorado ◽  
Blanca Irene Aldana ◽  
Sandra Adela Orozco-Suárez ◽  
Luisa Rocha
Keyword(s):  
Blood Brain Barrier ◽  
Neurological Disorders ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Histaminergic System ◽  
Blood Brain

scholarly journals Alzheimer’s disease: A matter of blood–brain barrier dysfunction?

2017 ◽  
Vol 214 (11) ◽  
pp. 3151-3169 ◽  
Author(s):  
Axel Montagne ◽  
Zhen Zhao ◽  
Berislav V. Zlokovic
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Amyloid Β ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Neurodegenerative Process ◽  
Blood Brain ◽  
Underlying Mechanisms

The blood–brain barrier (BBB) keeps neurotoxic plasma-derived components, cells, and pathogens out of the brain. An early BBB breakdown and/or dysfunction have been shown in Alzheimer’s disease (AD) before dementia, neurodegeneration and/or brain atrophy occur. However, the role of BBB breakdown in neurodegenerative disorders is still not fully understood. Here, we examine BBB breakdown in animal models frequently used to study the pathophysiology of AD, including transgenic mice expressing human amyloid-β precursor protein, presenilin 1, and tau mutations, and apolipoprotein E, the strongest genetic risk factor for AD. We discuss the role of BBB breakdown and dysfunction in neurodegenerative process, pitfalls in BBB measurements, and how targeting the BBB can influence the course of neurological disorder. Finally, we comment on future approaches and models to better define, at the cellular and molecular level, the underlying mechanisms between BBB breakdown and neurodegeneration as a basis for developing new therapies for BBB repair to control neurodegeneration.

Sign in / Sign up

Export Citation Format

Share Document