Alzheimer’s as a Contagious Prion Disease

Via ScienceDaily: New research shows that Alzheimer’s disease may in fact be able to spread between individuals in the same fashion as a prion disease.

You may have heard about prions in the news during the recent outbreak of mad cow disease (bovine spongiform encephalopathy). Prions are infectious proteins – a very counterintuitive idea, since we’re used to infectious agents being fungi, bacteria or viruses, as opposed to a single molecule.

Proteins fold into specific configurations that determine their function. A prion is the misfolded form of a certain type of protein, called PrP, that’s very widespread throughout the bodies of humans and other animals. When it comes into contact with the normal form of PrP, it somehow induces misfolding. In this way prions spread, and they end up aggregating into plaques that disrupt the nervous system. (Since it’s Nobel week, I should mention that the discovery of prions led to a Nobel prize in 1997.)

Alzheimer’s disease is also (possibly, not certainly) caused by the formation of plaques by proteins – called amyloid beta – in the nervous system. Now, research from the University of Texas Health Science Center at Houston shows that when brain tissue from human sufferers of Alzheimer’s disease is injected into healthy mice, the mice start developing their own plaques and Alzheimer’s-like symptoms, indicating that these plaques may in fact spread like prions. 

Of course, whether or not this has any impact on human health is still unclear. No one is accidentally inheriting diseased brain tissue from one another, to the best of my knowledge. Still, it’s always possible that misfolded amyloid beta is somehow being transmitted between individuals. If that’s true, it’d be a huge, huge discovery for the study of Alzheimer’s, a disease that affects a very large proportion of the elderly.    

(Edit: Interestingly enough, another article from today discusses how another protein that abnormally aggregates in relation to a neurological disease – alpha synuclein, in Parkinson’s and other diseases – may similarly recruit proteins in other cells to aggregate and spread the disease. This was seen within one organism, though, not spreading between organisms like a prion disease.)


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