Imbalance of iron homeostasis is a common feature of prion disease-affected human, mouse, and hamster brains, according to a new study by Dr. Neena Singh and colleagues at Case Western Reserve University School of Medicine, alongside collaborators from Creighton University.

In the rogues' gallery of microscopic infectious agents, the prion is the toughest hombre in town.

A worldwide group of scientists has created an infectious prion disease in a mouse model, in a step that may help unravel the mystery of this progressive disease that affects the nervous system in humans and animals.

Researchers from the National Institutes of Health and the Scripps Research Institute have found novel prion infectivity in white and brown fat tissues of mice. The study appears December 5 in the open-access journal PLoS Pathogens.

A comprehensive mouse model of inherited prion disease exhibits cognitive, motor, and neurophysiological deficits that bear a striking resemblance to the symptoms experienced by patients with the human version of "mad cow disease," Creutzfeldt-Jakob disease (CJD).

Prion protein, a form of protein that triggers BSE, is associated with other brain diseases in cattle, raising the possibility of a significant increase in the range of prion disease.

Prions, the infamous agents behind mad cow disease and its human variation, Creutzfeldt-Jakob Disease, also have a helpful side. According to new findings from Gerald Zamponi and colleagues, normally functioning prions prevent neurons from working themselves to death. The findings appear in the May 5th issue of the Journal of Cell Biology.

Researchers from the United Kingdom and France have identified four separate biochemical subgroups in a selection of cases of Creutzfeldt-Jakob disease. The study, published March 14th in the open-access journal PLoS Pathogens, suggests that these subgroups could represent distinct prion strains in what is the most common human prion disease.

In an advance in food safety, researchers in New York are reporting development of a nano-sized sensor that detects record low levels of the deadly prion proteins that cause Mad Cow Disease and other so-called prion diseases.

Prion infection of neurons increases the free cholesterol content in cell membranes. A new study published in the online open access journal BMC Biology suggests that disturbances in membrane cholesterol may be the mechanism by which prions cause neurodegeneration and could point to a role for cholesterol in other neurodegenerative diseases.

One of the new in vitro tests, called the Standard Scrapie Cell Assay, measures prion infectivity levels in a highly accurate and extremely rapid way, producing results in less than two weeks. The second test, called the Cell Panel Assay, allows researchers to quickly distinguish between several prion strains in various cells lines.

Lymph nodes can be crucial for spreading low doses of infective prion agents -the pathogens responsible for conditions such as scrapie and Creutzfeldt-Jakob disease - into the nervous system, according to new research published in the online open access journal BMC Veterinary Research.