Background:
Microglia play a pivotal role in maintaining homeostasis in complex brain environment.
They first exist as amoeboid microglial cells (AMCs) in the developing brain, but with brain maturation, they
transform into ramified microglial cells (RMCs). In pathological conditions, microglia are activated and have
been classified into M1 and M2 phenotypes. The roles of AMCs, RMCs and M1/M2 microglia phenotypes especially
in pathological conditions have been the focus of many recent studies.
Methods:
Here, we review the early development of the AMCs and RMCs and discuss their specific functions
with reference to their anatomic locations, immunochemical coding etc. M1 and M2 microglia phenotypes in
different neuropathological conditions are also reviewed.
Results:
Activated microglia are engaged in phagocytosis, production of proinflammatory mediators, trophic
factors and synaptogenesis etc. Prolonged microglia activation, however, can cause damage to neurons and oligodendrocytes. The M1 and M2 phenotypes featured prominently in pathological conditions are discussed in
depth. Experimental evidence suggests that microglia phenotype is being modulated by multiple factors including
external and internal stimuli, local demands, epigenetic regulation, and herbal compounds.
Conclusion:
Prevailing views converge that M2 polarization is neuroprotective. Thus, proper therapeutic designs
including the use of anti-inflammatory drugs, herbal agents may be beneficial in suppression of microglial activation,
especially M1 phenotype, for amelioration of neuroinflammation in different neuropathological conditions.
Finally, recent development of radioligands targeting 18 kDa translocator protein (TSPO) in activated microglia
may hold great promises clinically for early detection of brain lesion with the positron emission tomography.
TLR2 controls random motility, while TLR7 regulates chemotaxis of microglial cells via distinct pathways
