Identifying disease links
(Edmonton) Medical researchers at the University of Alberta have made further links between Alzheimer’s and prion diseases.
Co-investigator Jack Jhamandas, a researcher in the Division of Neurology within the Faculty of Medicine & Dentistry, said that the findings reveal for the first time that neurons affected by Alzheimer’s are impacted by a specific type of prion protein. He stressed these findings do not mean that Alzheimer’s is transmissible.
The research discovered that beta amyloid protein, which is deposited in large quantities in the brains of Alzheimer’s patients and is toxic to brain cells, ultimately causing these cells to die, may have interactions with a prion protein called PrPC. Well-known prion diseases include Creutzfeldt-Jakob disease and bovine spongiform encephalopathy (BSE or “mad cow disease”).
“Our interest is in where and how this interaction between the two proteins is taking place at a molecular level and to find some way to possibly modify it,” says Jhamandas.
“This is a significant finding. We are always looking for fundamental principles or experimental findings in biology that tie different diseases together. There are many neurodegenerative diseases, where at least one or more proteins have been identified as the culprits that facilitate progression of these diseases,” he said.
“Any findings that attempt to in some way link together these proteins advance our knowledge and hopefully treatment of these diverse groups of neurodegenerative diseases.”
The medical research community made initial connections between Alzheimer’s and prion diseases about two years ago. But the U of A findings take these connections one step further by studying the cells that are the target of current, albeit imperfect remedies, for Alzheimer’s.
“The findings show that Alzheimer’s disease and prion disease have unexpected common ground at the molecular level,” says co-investigator David Westaway, a researcher in both the Division of Neurology and the Centre for Prions and Protein Folding Diseases at the University of Alberta.
“We all have a normal prion protein in our brain cells, but this specific protein has a second life where it can become an accessory in the events of Alzheimer’s disease, impacting a specific population of cells very important to Alzheimer’s. The prion protein is itself a bit of an enigma, so we have to look at which part of that molecule mediates this impact in Alzheimer’s.”
Westaway stressed it is always important to identify new avenues of research because “you have to load the decks with fresh ways to intervene, so that at least some methods survive the gauntlet of stringent clinical testing.”
Their research was funded by the Alberta Prion Research Institute and PrioNet Canada. They are continuing their work in this area. The findings were being published in the peer-review publication Journal of Neuroscience Nov. 8.