Early glutathione intervention educed positive correlation between VGLUT1 expression and spatial memory in the Nω-nitro-L-arginine methyl rat model of IUGR.

Introduction: One of the most compelling causes of perinatal mortality and morbidity is intrauterine growth restriction (IUGR). IUGR is linked with numerous health challenges that last lifelong, including neurodevelopmental impairment and a high incidence of brain dysfunction. There is mounting evidence that places the glutamatergic system at the center of the neurobiology and treatment of neurological diseases.

Placental 11β-HSD2 downregulated in HIV associated preeclampsia.

Preeclampsia (PE) and human immunodeficiency virus (HIV) have been linked with marked increases in maternal stress, resulting in a significant change in placental function ranging from alterations in placental structure to the precise and delicate transformations in placental gene expression. Such changes may lead to altered transport of essential signals to the fetus, which can have long-term impacts on offspring health and consequently affect fetal neurodevelopment. Therefore, this work investigated the role of placental 11β-hydroxysteroid dehydrogenase types 2 (11β-HSD2) in HIV associated preeclampsia.

Amyloid-beta (1-42) lesion of CA1 rat dorsal hippocampus reduces contextual fear memory and increases expression of microglial genes regulating neuroinflammation.

Emerging evidence indicates that the pathogenesis of Alzheimer's disease (AD) is not confined to neuronal disruptions but robustly communicates with the brain's immune system. Genome-wide analysis suggests that several genes, which increase the risk for AD, encode for factors that regulate the glial clearance of misfolded proteins and the inflammatory reaction. This study reappraises the amyloid hypothesis by focusing on the impact of neuroinflammation in a beta-amyloid model of AD, how this possibly exacerbates the disease's progression, and the correlation between genes regulating neuroinflammation (CD33 and TREM2) with post-training recall.

Memory decline correlates with increased plasma cytokines in amyloid-beta (1-42) rat model of Alzheimer's disease.

Dysregulation of inflammatory markers like cytokines is implicated in the pathophysiology of Alzheimer's disease (AD). Altered level of these cytokines show that pathogenesis of AD is beyond dysfunction of neurons resulting from amyloid beta accumulation but involves neuroinflammatory mechanisms elicited by the neuroimmune cell. In this study, we investigated the effect of amyloid-beta (1-42) (Aβ) on memory and how inflammatory markers respond to this model of AD.