Background: Chronic neuroinflammation caused by activation of microglia and astrocytes in the brain contributes to neuronal loss and disease progression in Alzheimer's disease (AD). Recent research has identified type 2 diabetes mellitus (T2DM) as a risk factor for AD. High blood glucose (hyperglycemia) and the phenomenon of insulin resistance are being considered as the major factors contributing to an increased risk of AD.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the most common form of dementia worldwide. Type 2 diabetes (T2D) has been implicated as a risk factor for AD. Since T2D is a peripheral inflammatory condition, and AD brains exhibit exacerbated neuroinflammation, we hypothesized that inflammatory mechanisms could contribute to the observed link between T2D and AD.
View Article and Find Full Text PDFProblem-based learning (PBL) was originally introduced in medical education programs as a form of small-group learning, but its use has now spread to large undergraduate classrooms in various other disciplines. Introduction of new teaching techniques, including PBL-based methods, needs to be justified by demonstrating the benefits of such techniques over classical teaching styles. Previously, we demonstrated that introduction of tutor-less PBL in a large third-year biochemistry undergraduate class increased student satisfaction and attendance.
View Article and Find Full Text PDFIn vitro cultures of various glial cell types are common systems used to model neuroinflammatory processes associated with age-dependent human neurodegenerative diseases. Even though most researchers choose to use neonatal rodent brain tissues as the source of glial cells, there are significant variations in glial cell functions that are species and age dependent. It has been established that human and swine immune systems have a number of similarities, which suggests that cultured porcine microglia and astrocytes may be good surrogates for human glial cell types.
View Article and Find Full Text PDFThe effect of a moderate, physiologically relevant rise in temperature on several neuroinflammatory parameters was investigated in vitro using human cell lines and cultured human astrocytes. A two degree Celsius rise in temperature was found to enhance the neurotoxicity of microglia-like and astrocytic cells, increase the release of monocyte chemotactic protein (MCP)-1 by activated human monocytic THP-1 cells and amplify the generation of reactive oxygen intermediates by differentiated HL-60 myelocytic cells. Moderate increases in body temperature may exacerbate neuroinflammation and neuronal injury in chronic neurodegenerative disorders.
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