The research associated with this dataset explored cross-species prion transmission and the impact of cofactor environment on strain adaptation. Utilizing Protein Misfolding Cyclic Amplification with beads (PMCAb), hamster strain 263K was propagated under normal or RNA-depleted conditions first in mouse and then hamster substrates. A variety of readaptation experiments were conducted including brain analysis of hamsters inoculated with different PMCAb-derived material. Dataset includes Western blot and comparative histopathological brain images.
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.