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During decades, glia cells have been considered such as protective and nutrient cells taking care neurons in the brain.
In this decade, many scientists have published different roles for astrocytes, oligodendroglia, microglia and endothelial
cells. The main aim of this study was to show the role of glia in Alzheimer�s disease using transgenic APP/Presenilin 1 and
comparing with Wild type mice. We detect increase in inflammatory genes in wild type mice compared with transgenic one,
demonstrating a chronic inflammation in those mice. Also we noted increase in CCL3 and CCL4 genes involved in brain
demyelination compared with wild type mice, which can explain the cleaning job of astrocytes in transgenic mice trying
to eliminate A�²1-42 plates. By microarray CCR8, CX3CL1 and CXCR3 genes were significantly high expressed in wild type
compared with transgenic mice, showing us the proper positioning of activated T cells with adhesive, trafficking and migratory
functions in wild type. In fact we detect also a significant increase of IL-3 in transgenic mice compared to wild type indicating
activation of T cells and induction of proliferation and differentiation of T cells in transgenic mice compared with wild type. In
our study, integrin activation, cytoskeletal changes and chemotactic migration was also altered in transgenic mice compared
to wild type. For instants, astrocytes play important roles such as protector of neurons in front of inflammation imbalance
and regenerating damage intake. Further we detect presence of tumour resistant gene in transgenic mice, ABCF1, without any
expression of this gene in wild type and on the contrary expression of CCL12, cancer gene, in wild type without any expression
in transgenic mice. These last data indicate a resistance of transgenic mice to cancer compared to wild type mice. In the future
the study of the communication between all brain cells will be necessary to understand much neurodegenerative illness and
the protection of stem natural cells of our young brain will be the next frontier.