The activation of
complement system is important factor in inflammatory, neurodegenerative and
cerebrovascular diseases. CNS cells are able to synthesize
complement components, and myelin and oligodendrocytes (OLG) are known to activate the classical pathway of
complement in vitro in the absence of
antibodies. Although activation of the
complement system is known to promote tissue injury, recent evidence has also indicated that this process can have
neuroprotective effects. In particular, terminal
C5b-9 complexes enhance OLG survival both in vitro and in vivo. Complement activation may also reduce the accumulation of
amyloid and degenerating neurons by promoting their clearance and suggest that certain inflammatory defense mechanisms in the brain may be beneficial in
neurodegenerative disease.
Complement system activation plays also an important role in brain damage after ischemic injury or
head trauma. These findings strongly suggest that complement activation and membrane assembly of
C5b-9 can play a role in injury but can also provide neuroprotection depending on the pathophysiological context.