Autor/es reacciones

Andrew Doig

Professor of Biochemistry and Programme Director for Biochemistry, University of Manchester

Does the press release accurately reflect the science?

“Generally, yes. However these final conclusions, based on the abstract, are very speculative: “However, they note that the recognition of amyloid-beta transmission emphasizes the need to review measures to prevent accidental transmission via other medical treatments and procedures. These findings could have implications for the processes that drive other types of Alzheimer’s disease and may provide insights into therapeutic strategies, they conclude.” 

There is no evidence that the mode of disease transmission presented here (transmission by) has ever occurred elsewhere. We are already very careful about transmitting brain tissue between people, due to the small but real risk of passing on prions which might cause CJD.

There is evidence that amyloid-beta aggregates can travel across synapses in the brain, spreading dementia. This work adds support to this idea. Whether the work has any implications for therapeutic strategies remains to be seen. The paper speculates on whether different strains of amyloid-beta are present, resulting from different aggregate structures, but present no direct evidence for this".

Is this good quality research?  Are the conclusions backed up by solid data?

“Yes, the work is thorough and carefully done. As discussed above, the discussion on the need for new procedures, the existence of strains and implications for therapies are speculative and lack evidence. Otherwise, the conclusions are reasonable, but we must bear in mind that only 8 patients are considered".

How does this work fit with the existing evidence?

“Previous work has shown that aggregates of amyloid-beta could be transmitted to humans along with human growth hormone, though we did not know whether they had any effects. This new work suggests for the first time that these aggregates can indeed cause a disease resembling Alzheimer’s".

Have the authors accounted for confounders?  Are there important limitations to be aware of?

“It is well known that early onset Alzheimer’s can be caused by mutations in the PSEN1, PSEN2 or APP genes. This does not seem to be the case here. Other possible explanations for the Alzheimer’s symptoms are intellectual disability in the patients, other linked diseases, growth hormone deficiency or effects of radiotherapy. All were ruled out, leaving Alzheimer’s transmission from the growth hormone treatment as the best explanation for the disease symptoms. One must be cautious, however, as only 8 patients are considered and some data for them in incomplete, such as the genetics.

It is important to emphasise, however, that these symptoms seem to have arisen from a medical procedure that was last used in 1982".

What are the implications in the real world?  Is there any overspeculation?

“While the new type of Alzheimer’s reported here is of great scientific interest, as it reveals a new way to spread the disease, there is no reason to fear it, as the way in which the disease was caused was stopped over 40 years ago. Disease transmission from human brain to brain in this way should never happen again".

EN