**6. Conclusions**

Astrocytic changes have been linked to SCZ at the neurobehavioral, structural, functional, and molecular levels. ECM, gap junctions, and epigenetics are also


#### **Table 2.**

*A summary of important points from this chapter.*

implicated in the astrocytic abnormalities associated with SCZ. Various neurotransmitter systems that are regulated by astrocytes including GABA, glutamate, and adenosine are involved in SCZ. Also, different types of neuroplasticity governed by astrocytes are altered in SCZ. Moreover, hyperinflammation that is in part regulated by astrocytic inflammasomes (e.g., NLRPs) is present in SCZ patients and is affected by pharmacotherapy with antipsychotics. Clinical behavioral deficits in animal models are also related to aberrancies in astrocytes. When taken together, the plethora of studies that indicate a link between astrocytic dysfunction and SCZ should warrant future research to explore the role played by astroglial cells in SCZ to bridge the clinical and molecular findings and pave the path for developing future therapeutics that correct, or exploit, astrocyte functions in SCZ (**Table 2**).
