Optimization of intracerebroventricular streptozotocin dose for the induction of neuroinflammation and memory impairments in rats.

Intracerebroventricular (ICV) injection of streptozotocin (STZ) is a well established procedure to induce neuroinflammation leading to dementia in experimental animals. However, the optimal dose of STZ has not been determined. In the present study, rats were ICV injected with 1.

Intracerebroventricular Aβ-Induced Neuroinflammation Alters Peripheral Immune Responses in Rats.

An important marker in Alzheimer disease (AD) is the abnormal production and accumulation of β-amyloid peptide (Aß) in brain. It produces oxidative damage in neurons and inflammation due to its neurotoxic properties. The present study was designed to investigate neuroinflammation (hippocampal levels of ROS, nitrite, TNF-α, and IL-1β), neurodegeneration (plaques and chromatolysis in hippocampus), and memory impairments (working memory and reference memory) and the effect of this neuroinflammation on some peripheral immunological parameters such as phagocytic activity of blood WBC and splenic polymorphonuclear (PMN) cells, leucocyte adhesion inhibition index (LAI), and cytotoxicity of splenic mononuclear cells (MNC) after the intracebroventricular injection of aggregated Aβin a 4week study.

Nitric oxide synthase inhibitor, aminoguanidine reduces intracerebroventricular colchicine induced neurodegeneration, memory impairments and changes of systemic immune responses in rats.

Intracerebroventricular (i.c.v.

Dual Role of Vitamin C on the Neuroinflammation Mediated Neurodegeneration and Memory Impairments in Colchicine Induced Rat Model of Alzheimer Disease.

The neurodegeneration in colchicine induced AD rats (cAD) is mediated by cox-2 linked neuroinflammation. The importance of ROS in the inflammatory process in cAD has not been identified, which may be deciphered by blocking oxidative stress in this model by a well-known anti-oxidant vitamin C. Therefore, the present study was designed to investigate the role of vitamin C on colchicine induced oxidative stress linked neuroinflammation mediated neurodegeneration and memory impairments along with peripheral immune responses in cAD.

NMDA receptor is involved in neuroinflammation in intracerebroventricular colchicine-injected rats.

The neurodegeneration in intracerebroventricular (icv) colchicine injected (ICIR) rats is linked with neuroinflammation. Glutamate excitotoxicity through NMDA receptors is involved with the neuroinflammation in some animal models of Alzheimer Disease (AD), but it has not been explored in ICIR rats. The aim of this study was to investigate the role of NMDA receptors (by blocking it's activity with memantine) in colchicine-induced neuroinflammation and neurodegeneration and impacts on peripheral immune parameters in ICIR rats.

A comparison of neurodegeneration linked with neuroinflammation in different brain areas of rats after intracerebroventricular colchicine injection.

Colchicine induces neurodegeneration, but the extent of neurodegeneration in different areas of the brain in relation to neuroinflammation remains unclear. Such information may be useful to allow for the development of a model to compare colchicine-induced neurodegeneration with other neurodegenerative diseases such as Alzheimer's Disease (AD). The present study was designed to investigate the extent of neurodegeneration along with neuroinflammation in different areas of the brain, e.