Chronic neuroinflammation is a common pathological hallmark of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS, and prion disorders. Both reactive microgliosis and astrogliosis have been identified as having a role in the neuroinflammatory process. Studies of prion diseases of animals and humans have demonstrated activation and proliferation of microglia at the very early subclinical stages. Less is known about the role of reactive astrocytes. This research investigated the changes in normal functions of astrocytes over the course of chronic neuroinflammation including their region-specific responses in the brain. Studies of brain tissue of mice infected with 22L mouse-adapted prion strain include histological, immunofluorescence, and qRT-PCR. Prion deposition and reactive microgliosis and astrogliosis were examined across regions of the whole brain with particular focus on the thalamus and hippocampus.
A high glucose level associated with maternal diabetes has been identified as a risk factor for fetal neural tube defects (NTD). The failure to successfully complete the complex neurulation process is possibly related to the loss of protection for cellular homeostasis resulting in organelle stress. Mitochondrial dysfunction and endoplasmic reticulum stress in the developing endothelium have been identified as significant components in diabetic embryopathy. Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) is a critical protein involved in fetal neural development. This study investigated the regulation and biological activity of MARCKS and its role in protecting neuroepithelial cell organelles during neurulation. Furthermore, the effects of the acetylation/phosphorylation/deacetylation of MARCKs by Tip60 and sirtuin 2 were examined with respect to the protein’s protective functionality. The dataset includes immunoblot/immunofluorescent/electronmicroscopy images and graphs.