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Advanced Neurology Microglia in autism spectrum disorder

Figure 4. Targeted treatment of immune activation in pregnancy. In the early stage of pregnancy, the exposure of the mother to external stimuli, such as
rubella virus, bacteria, and Toxoplasma, leads to the activation of microglia and the maternal immune system, as well as an increased secretion of cytokines.
Treatments that are commonly used include the prevention and removal of pathogens to reduce maternal infection by stimulating the immune system
and inhibiting maternal immune activation signaling; a concomitant administration of anti-interleukin (IL)-6 and -IL-1β antibodies in poly(I: C) models
could take effect in animal models.

biomarkers of response to treatment [73,74] . A timely analysis and CNS of autistic patients. Insights into possible targets
of gestational samples is an excellent opportunity for associated with microglia would aid the development of
pathological diagnosis and future behavioral interventions potential medical therapies for various CNS disorders.
in the early ASD childhood. However, the average age of A recent study identified a novel pharmacological anti-
ASD children at which atypical behaviors are first noticed neuroinflammatory agent and GIBH-130, for Alzheimer’s
by the parents is 4.6 years . This means that sample disease through microglia-based phenotypic screening,
[75]
analysis during pregnancy may not be a suitable solution the method by which novel favorable targets in ASD
due to parental acceptance. Some animal experiments have models may be introduced . Further studies are needed
[77]
shown promising results concerning therapeutic targeting to confirm the specificity of inflammatory factor release
T helper 17 (Th17) cells in preventing inflammation- and the intricate interactions between microglia and
induced ASD-like behaviors in offspring of susceptible inflammation. Besides, glial cell modulation cannot be
mothers . However, the specific inflammatory factors precisely controlled, and microglia modulation may have
[76]
that cause ASD are poorly understood, and most existing other adverse effects on the CNS, thus posing a challenge
immunomodulatory tools are ineffective. There are still for ASD treatment.
many challenges in reversing the pathological changes in
gestation to ameliorate ASD-like behaviors in offspring; 6. Conclusion
however, fostering routine sample analysis and clinical Our work offers a summary of the main pathological
trials would help address these challenges. mechanisms of microglia in ASD and several targeted
Microglia are innate immune cells of the CNS. An therapeutic methods. There are limitations in the existing
important pathogenic mechanism of ASD is the decreased mechanisms, such as the ambiguous pruning preference
ability of microglia to engulf and prune unwanted for which type of synapses and the lack of explicit cause-
synapses, resulting in CNS inflammation. A number of effect relationship between studies, like MIA and microglia
studies have demonstrated that microglia release IL-1β, polarization. Focusing on new insights such as glial cell
IL-6, IL-8, and other inflammatory factors, and these interactions and autophagy may bring promising results. As
factors are significantly increased in the peripheral blood for effective interventions, most therapeutic methods are still

Volume 1 Issue 3 (2022) 8 https://doi.org/10.36922/an.v1i3.167