Topic: maternal immune activation

Background: Past studies have revealed the lasting effects of stress susceptibility and maternal immune activation on hippocampal DNA methylation landscape in adult offspring. Yet, alterations of the DNA methylation landscape during early postnatal development and following maternal immune activation remain less studied. Methods: We used two mouse strains characterized by social dominance (Dom) and submissiveness (Sub), exhibiting inherent traits of elevated and diminished stress sensitivity. Additionally, Poly IC was administered to a subgroup of the dams at gestational day 14 to induce mater

Neurodevelopment is a highly orchestrated and precisely timed process that displays vulnerability towards environmental insults. Maternal immune activation (MIA) during gestation can disturb this delicate balance and increase the offsprings risk for neurodevelopmental disorders like schizophrenia and autism later in life.This study investigates the differential impact of MIA on neuronal progenitor cells at E10.5 (polyI:C administration at E9.5) by using single-cell RNA sequencing. Additionally, we examined the role of microglia in mediating the effects of MIA at different developmental stages.

Maternal infections and prenatal inflammation are recognized risk factors for neurodevelopmental diseases. Astrocytes are glial cells essential for synapse formation and refinement, but they also may react to inflammatory environment affecting neuronal network homeostasis. However, how an inflammatory episode occurring during fetal development influences astrocyte generation and phenotype remains largely unknown.In the brain, the innate immune molecule Pentraxin3 (PTX3) is produced by astrocytes and promotes the maturation of excitatory synapses. Its expression is induced by inflammatory stimu

Early episodic and contextual memories are forgotten despite their distinct impact on personality development and future behaviour. This phenomenon, termed infantile amnesia, is widely seen in humans and is conserved across other altricial species. In previous years it has become evident that infant memories are stored through the plasticity of neuronal ensembles, forming engrams that remain present in the brain in a latent state once forgotten. Recently, it has been shown that alterations in brain development caused by maternal immune activation (MIA) lead to infant memory retention in male o

Maternal influenza infections pose a significant risk for neurodevelopmental disorders and have been linked to an increased incidence of autism and schizophrenia. While maternal immune activation is a well studied paradigm, most studies model only the acute stages due to use of synthetic viral mimetics. To investigate the impact of maternal influenza infection during pregnancy, we exposed pregnant mouse dams to influenza strains (dose of 1-3 LD50) with different virulence. Pregnant mice were exposed at different stages of gestation to understand whether cerebral cortical cell types showed diff

A growing body of evidence indicates a substantial role of the immune system and inflammation in the pathogenesis of Alzheimer’s disease (AD). In the current study, we investigated the effect of maternal immune activation (MIA) on AD-resembling pathological alterations in 12-month-old offspring. We also aimed to analyze whether inhibition of bromodomain and extraterminal domain (BET) proteins, the readers of the histone acetylation code, might impact these changes. In our study, we injected a viral mimetic polyinosinic-polycytidylic acid (PIC) at gestation day 17 to evoke MIA in wild-type mice

Maternal immune activation (MIA) has been implicated in offspring neurodevelopmental and psychiatric disorders, although it is unknown to what extent MIA affects neurodevelopment in the general population, and whether effects differ by sex. The current study was set within FinnBrain, a prospective birth cohort study based in Turku, Finland. We examined the association between maternal prenatal C-reactive protein (CRP), a commonly used systemic inflammatory marker, and white matter fractional anisotropy (FA) and mean diffusivity (MD) in infant and 5-year-old offspring, using voxel-wise statisti

Maternal exposure to viruses and related immunogens can have deleterious effects on neurodevelopment and lead to an increased risk of several psychopathologies, such as schizophrenia. Alcohol use disorder is more prevalent among individuals diagnosed with schizophrenia. However, the mechanisms underlying this association remain unknown. Here, we exposed pregnant rats to the viral analogue poly IC and studied several features of alcohol use disorder in the offspring, including increased motivation, compulsivity, and preference for ethanol over an alternative reward (saccharine). Prior to these

Introduction: Maternal immune activation (mIA) is a risk factor for schizophrenia. It is hypothesised that mIA-induced fetal neuroinflammation alters neurodevelopment and predisposes offspring to neuropathology. Using our validated mIA model, exposing pregnant rats to the viral mimetic poly(I:C), we have shown that adult offspring exhibit cognitive deficits comparable to those in schizophrenia, and have genomic methylation changes enriched for oligodendrocyte genes.Aims: Examine the relationship between mIA and altered oligodendrocyte development and how these correspond to the onset of adult

Gestational infection is considered as contributing factor for the development of psychopathologies later in life. The Maternal Immune Activation (MIA) mouse model, based on the systemic administration of the double-stranded RNA analogue Poly(I:C), is used to study the effects of gestational infection on offspring brain function and behavior.Previously, we demonstrated that stimulating pregnant mice with Poly(I:C) not only affects the developing brain in-utero, but also impacts on the structural and functional integrity of the maternal brain to disrupt maternal care behavior postpartum. Howeve

Aims: In the context of the maternal immune activation and neuroinflammation hypotheses of schizophrenia (SZ), we studied NLRP1 mRNA and protein expression in the postmortem brain tissue from a total of 10 SZ and 10 controls. Methods: RNA underwent reverse transcription and was hybridized onto the Affymetrix HG-U133 Plus 2.0 array, using the same protocol as the GeneChip Human Exon 1.0ST Arrays (Affymetrix, Santa Clara, CA, USA), which examines over a million exons, spanning 17,868 NCBI RefSeq transcripts. Brain tissue samples were embedded in paraffin, cut into 12 μm-thin sections, and subjec