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.

In work originating from the Bavarian Research Cooperation Prions (FORPRION), which ended in 2007, a team led by the scientist Prof. Dr. Christine Leib-Mösch has been able to show that prion proteins may activate endogenous retroviruses in infected brain cells.

Researchers have provided new information about how communication among neurons may be prevented from deteriorating in conditions such as Alzheimer’s disease (AD). The new results may lead to new therapies for the treatment of not only AD but also motor neuron diseases and prion diseases.

Scientists have discovered a new protein that may offer fresh insights into brain function in mad cow disease. “Our team has defined a second prion protein called ‘Shadoo’, that exists in addition to the well-known prion protein called ‘PrP’ ” said Professor David Westaway, director of the Centre for Prions and Protein Folding Diseases at the University of Alberta.