Peripheral T Cells Response To β-Amyloid Peptide Deposition In Rat Brain

Alzheimer' s disease ( AD) is an age - related chronic neurodegenerative disorder, seriously affecting the senior people' s living conditions. It is important to understand the pathogenesis of AD and explore the therapeutic strategies. A potential model is essential for the study of AD pathology.Genetic, pathologic, and animal studies suggest that beta - amyloid protein ( Aβ) deposits play a central role during early - stage of AD. It is believed that aggregated Aβ exerts neurotoxicity and initiates the progressive pathophysiology of AD, including comprehensive microgliosis and astrogliosis, inflammatory mi-croenvironment and neuronal cell dysfunction and cell death.A prominent innate immune response occurs in the central nervous system in association with Aβ deposition. The recruitment of circulating immune cells to inflammatory lesions by proinflammatory cytokines producing in the process of innate immune responses may lead to the initiation of subsequent adaptive immune responses. Initiation and regulation of immune cell trafficking through blood - brain barrier ( BBB) is a crucial step and is poorly understood. The blood - brain barrier, composed of parenchymal microvascular endothelia cells, basement membrane and foot processes of astrocytes, restricts the free passage of cells and molecules from systemic compartment into the central nervous system ( CNS). However, several lines evidences suggest that, even under physiologic conditions, immune surveillance is ongoing process within CNS and is achieved preferentially by lymphocytes with an activated phenotype to clear the possible pathogen.