Is it possible for Alzheimer’s to be transmitted by tissue or fluid transfers between people? Last September, John Collinge, a British professor of neurology, raised this possibility in a controversial paper published in the journal Nature.

In this paper, Collinge reported on the autopsy of four of patients who had been injected with human growth hormone (HGH) as children and who subsequently contracted Creutzfeldt-Jakob Disease (CJD). He found that all four not only had prions, but also amyloid beta plaques, considered a hallmark for Alzheimer’s. He posited that tissue of a donor could contain  transmittable “seeds” of Abeta protein, which over time would result in the development of Alzheimer’s in the recipient.

There are profound implications if this possibility is borne out. However, it is important to note that none of the patients autopsied had any tau protein, increasingly considered necessary for Alzheimer’s expression, nor did any of the patients show signs of cognitive impairment.  Further, medical science has advanced to the point where cadaver derived substances, such as the HGH used on the four patients in question, have been replaced with synthetic versions.

Nonetheless, scientists around the world have been working to verify Collinge’s findings. In January, scientists in Switzerland announced that they had examined the brains of 7 subjects who had received surgical grafts of cadaver derived dura – membranes that cover the brain and spinal cord, all of whom developed CJD.  They discovered that 5 of the 7 also had Abeta deposits in their brains.

Last week, Nature published an update on research into the transmissibility of Abeta.  reported further examination of this theory.   It suggests that the answers will be a long time in coming, as large populations will need to be studied to determine if there is a causal relationship.  The work will be hindered by the fact that neither prion disease nor Alzheimer’s is well understood.

Critics argue that it is far too soon to assume any propensity for transmissibility, and note the following:

1. The size of the study samples to date are far too small to be conclusive.
2. The subjects who had Abeta deposits had no signs of cognitive impairment prior to their death.
3. There is no epidemiological evidence to suggest that asymptomatic Alzheimer’s patients have been transmitting the disease through blood donations or contaminated surgical instruments.
4. The existence of  Abeta “seeds” is only a theory.
5. The lead investigator has a conflict of interest because he is both a director and a shareholder in a biopharmaceutical company that is developing antibodies against prions and selling a prion decontamination product.

The bottom line is that neither CKD nor Alzheimer’s is well understood, and certainly there is not enough data to conclude that Alzheimer’s is transmissible. On the other hand, researchers know that both diseases are tied to abnormal proteins, and that there may be much to be jointly learned about the brain and its diseases by joining forces in research.