No warning for this Scarlet A's approach |

What does it mean for us all if Alzheimer’s doesn’t originate in the brain?

That’s not as far-fetched an idea as you might think. After all, Creutzfeldt-Jacob disease (CJD) can be acquired by ingesting infected meat products- or even via blood transfusions. (These contain the contagion of prion proteins.)

Given that CJD involves a misfolded protein as a component of the brain disease- why not Alzheimer’s, which seems to involve beta-amyloids, another misfolded protein. And, we already know that amyloid plaques are associated with those who have the disease. (No, I am not going to reeducate us all about the difference between correlation and causation. You can find some knowledge here, though.)

So, when a study indicates that a mouse- a healthy one- which, when connected to a mouse replete with beta-amyloid plaques (indicating Alzheimer’s-like disease) can develop the plaques in its own brain, we panic. Because that plaque accumulation means the mouse’s heretofore healthy brain tissue begins to die. (Please note that mice don’t really develop Alzheimer’s; these mice were provided a gene that would let them produce the human version of the disease.)

That research was effected in the lab of Dr. Weihong Song, who holds the research chair in Alzheimer’s Disease at the University of British Columbia. He’s not alone in this finding, though. Dr. Larry Walker of the University of Georgia working with Mathias Jucker of the University of Tubingen also found they could induce Alzheimer’s by injecting the plaques into a healthy mouse’s peritoneum.

Song’s research group published their results in Molecular Psychiatry (http://www.nature.com/articles/mp2017204 ). Song traveled down this path because he knew that the beta-amyloid proteins are produced in peripheral tissues and can then be secreted into the circulating blood.

And, while the beta-amyloid accumulated in the mice brain, within four months the mice demonstrated altered brain activity in the learning and memory regions. Clearly demonstrating that the disease may be ‘carriable’ by blood transfusions.

Don’t panic yet about blood transfusions, though. Because Dr. Gustaf Edgren (Karolinska Institute) and his group examined some 2 million blood transfusion recipients (located in Denmark and Sweden). Their study failed to find any elevated risk of developing Alzheimer’s. Except (which means it can’t refute the hypothesis), the transfusions were not administered repeatedly to other patients or over long time periods (as was true for the conjoined mice studies) and this study may not have covered a sufficiently long time frame.

Tomorrow, we’ll continue our studies.