Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders.
Cynthia J M KanePaul D DrewPublished in: Journal of neuroscience research (2020)
Ethanol exposure to the fetus during pregnancy can result in fetal alcohol spectrum disorders (FASD). These disorders vary in severity, can affect multiple organ systems, and can lead to lifelong disabilities. Damage to the central nervous system (CNS) is common in FASD, and can result in altered behavior and cognition. The incidence of FASD is alarmingly high, resulting in significant personal and societal costs. There are no cures for FASD. Alcohol can directly alter the function of neurons in the developing CNS. In addition, ethanol can alter the function of CNS glial cells including microglia and astrocytes which normally maintain homeostasis in the CNS. These glial cells can function as resident immune cells in the CNS to protect against pathogens and other insults. However, activation of glia can also damage CNS cells and lead to aberrant CNS function. Ethanol exposure to the developing brain can result in the activation of glia and neuroinflammation, which may contribute to the pathology associated with FASD. This suggests that anti-inflammatory agents may be effective in the treatment of FASD.
Keyphrases
- induced apoptosis
- blood brain barrier
- spectrum disorder
- cell cycle arrest
- neuropathic pain
- oxidative stress
- endoplasmic reticulum stress
- anti inflammatory
- inflammatory response
- white matter
- traumatic brain injury
- signaling pathway
- risk factors
- lipopolysaccharide induced
- mild cognitive impairment
- gram negative
- patient safety
- brain injury
- resting state
- cerebrospinal fluid
- combination therapy
- pi k akt