Maternal immune activation and abnormal brain development across CNS disorders
Epidemiological studies have shown a clear association between maternal infection and schizophrenia or autism in the progeny.
Animal models have revealed maternal immune activation (mIA) to be a profound risk factor for neurochemical and behavioural abnormalities in the offspring.
Microglial priming has been proposed as a major consequence of mIA, and represents a critical link in a causal chain that leads to the wide spectrum of neuronal dysfunctions and behavioural phenotypes observed in the juvenile, adult or aged offspring. Such diversity of phenotypic outcomes in the mIA model are mirrored by recent clinical evidence suggesting that infectious exposure during pregnancy is also associated with epilepsy and, to a lesser extent, cerebral palsy in children.
Preclinical research also suggests that mIA might precipitate the development of Alzheimer and Parkinson diseases.
Here, we summarize and critically review the emerging evidence that mIA is a shared environmental risk factor across CNS disorders that varies as a function of interactions between genetic and additional environmental factors. We also review ongoing clinical trials targeting immune pathways affected by mIA that may play a part in disease manifestation. In addition, future directions and outstanding questions are discussed, including potential symptomatic, disease-modifying and preventive treatment strategies.
This is the one of the clearest and detailed explanations of how a Maternal Immune Activation across the varying stages of pregnancy can result in autism , schizophrenia, epilepsy. Previous research also suggests clinical anxiety , depression and bipolar disorder.
If you are at all interested in the gene x environment and how it works in ASD I urge you to read the full article at this link –
and read some of the past articles we have assembled over the years on this site