Upon activation by trauma, infec tion or any other neurodegenerative stimuli, microglia retract their ramifications, transform into amoeboid or spherical shape, produce pro inflammatory cytokines and display phagocytosis. These microglia are known to be activated or reactive. Studies nilotinib hcl in chronic, aging associated neuropathologies such as Alzheimers disease, and Parkinsons disease indicate persistent microglial activation as the major causative factor in disease Inhibitors,Modulators,Libraries exacerbation. Aging brains are often characterized by the presence of primed microglia, which present an altered cytokine profile in com parison to their counterparts in younger brains. These microglia produce an exaggerated inflammatory re sponse when activated leading to prolonged cycles of proliferation and production of pro inflammatory cytokines which eventually render them neurotoxic.

Fur ther, Inhibitors,Modulators,Libraries chronic microglial activation has been shown to cause the impairment of adult neurogenesis in hippocampus and damage to the periventricular white matter in the early postnatal brain. Hence activated microglia in both postnatal and adult stages can have neurotoxic effects on the CNS by causing excessive inflammation. Identification of ways to attenuate microglia mediated neuroinflammation, therefore, has been the primary consid eration in therapeutic strategy. There is accumulated infor mation on the factors that contribute to the activation, migration, proliferation and immune response of microglia over the years, but the gene expression and signal ing networks that function within these cells are yet to be fully clarified.

Gene expression profiles of microglia from primary cul tures are available, but their expression profiles have been found Inhibitors,Modulators,Libraries to be altered once isolated from their natural milieu. It is striking that investigation on the expression pro files of functioning genes of AMC and RMC in vivo in their quiescent state have remained elusive. In this connection, we carried out a global gene expression profiling of AMC and RMC in situ by isolating them from the CC of rat brain using laser capture microdissection tool. Overlap ping the transcriptome onto several online and commercial databases, our current study aimed to identify molecular candidates that are associated with the morphological transformation and physiological functioning of microglia Inhibitors,Modulators,Libraries in the developing brain.

Further, we have identified the genes that render stemness and monocytic functions to AMC and RMC. The transcriptome profiling has also led to the identification of several genes that may be vital in regulating microglial proliferation, differentiation, migra Inhibitors,Modulators,Libraries tion, and ramification. Methods Ethics statement In this research the handling and care of animals, the International Guid ing Principles for Animals Research, as adopted by the Institutional Animal Care and Use Committee, National University of Singapore, were followed.