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evidently implicated in regulation of learning and autophagy also influenced apoptosis of reactive
memory activity in CNS. Conditional removal astrocytes and down-regulation of autophagy
or down-regulation of these specific receptors caused time-dependent changes in extrinsic and
enhanced memory in aging or Alzheimer’s disease intrinsic apoptotic pathways, indicating that
(AD) animals, indicating abnormal increase of autophagy in astrocytes might also act as an early
adenosine receptor A2a in reactive astrocytes might adaptive response before initiation of apoptosis and
contribute to AD-linked memory loss. [8] necrosis. [15]

Reactive astrocytes may display a self- Taken together, we hypothesize that apoptosis of
regulativeapoptosis for modulation of over- reactive astrocytes may also possibly present a
activated astrocytes or functional balance in the self-regulator for those over-activated astrocytes
neuroinflmmatory event or diseased CNS. Cell or functional balance between neurotrophic and
apoptosis was earlier identified in the reactive inflammatory properties in neuroinflammation,
astrocytes, but its real significance remains while reactive astrocytes work actively as
unclear in the neuroinflammation and diseased aparticipator in astrocyte-microglial communication
conditions. Astrocytic apoptosis in vitro and in vivo and microglia-dominating inflammatory response.
2+
might attribute to Ca overload, mitochondrial Nevertheless, one critical question regarding this
dysfunction, oxidative stress and NF-κB signaling self-regulatory apoptosis of reactive astrocytes in
activation. It is known that obvious inflammatory ameliorating the neuroinflammatory injury should
[9]
injury of CNS neurons occur in pathogenesis of still merit further extensive investigations to
neurodegenerative diseases such as AD and PD. While elucidate its exact roles in pathogenesis and disease
the reactive astrocytes and microglial cells dominate progression of various neurological disorders.
in the inflammatory reaction, major histocompatibility
complex II (MHC II) levels were significantly up- Financial support and sponsorship
regulated in midbrain of 1-methyl-4-phenyl-1,2,3,6- Supported by grants from the National Natural
tetrahydropyridine (MPTP) model of PD and MHC II Science Foundation of China (31371374) and the
was mainly localized in astrocytes and microglia, in National Basic Research Program (2012CB525002).
which MHC II mediated T cell activation in initiating
immune reaction and in participating disease Conflicts of interest
[10]
progression. Besides, astrocyte activation and There are no conflicts of interest.
apoptosis was observed in lipopolysaccharide (LPS)-
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168 Neuroimmunol Neuroinflammation | Volume 3 | July 20, 2016