The Brain

More Evidence Suggests Protein Linked To Alzheimer’s May Be Transmissible

January 28, 2016 | by Ben Taub

Amyloid beta plaques were found in the brains of dura mater transplant recipients
Photo credit: Amyloid beta plaques were found in the brains of dura mater transplant recipients. Juan Gaertner/Shutterstock

A study has indicated that proteins linked to Alzheimer’s disease might be transmissible during surgical transplants, adding to the evidence provided by separate research that reached the same conclusion last September. While both studies suggest that these so-called amyloid beta proteins may be somehow “seeded” in a patient’s brain as a result of medical procedures, this does not necessarily mean that recipients will go on to develop Alzheimer’s, as much is still unknown about what causes the condition.

The accumulation of amyloid beta proteins into brain plaques that impede neurological function is a key marker of Alzheimer’s, although this is rarely seen before old age. However, a paper that appeared this week in Swiss Medical Weekly has revealed that these plaques were found in the brains of young people and adults – aged 28 to 63 – who had received dura mater transplants. Dura mater is the membrane surrounding the brain and spinal cord, and used to be transplanted in the form of grafts in order to repair the membranes of patients who underwent brain surgery. These days, synthetic membranes are used for this purpose.

The seven subjects involved in the study all later died as a result of a neurodegenerative disease called Creutzfeldt-Jakob Disease (CJD), which is caused by a rogue, misfolded form of a normal protein called the prion protein. Subsequent investigations revealed that this protein had been transferred along with the dura mater they received during their transplants.

Conducting autopsies on these seven brains, the study authors discovered that five of them contained amyloid beta plaques, despite the fact that all subjects had died at an age much younger than that typically associated with the development of these plaques. This led them to propose that fragments of these proteins may have been transferred along with the dura mater, and “seeded” in their brains.

A similar suggestion was made by the authors of another recent study that looked at the brains of deceased human growth hormone recipients. Transplants of this hormone – which is extracted from the pituitary glands of deceased donors – was halted in 1985, after it too was found to carry a risk of transferring pathogenic prion proteins.

The autopsies carried out during this study also revealed the presence of amyloid beta plaques in brains that would normally be considered too young to have developed them. As such, the researchers suggested that certain compounds leading to the formation of these plaques may have been transplanted along with the human growth hormone.

The findings of both studies have caused considerable debate, and while these transplants represent just one of several possible explanations for the presence of amyloid beta proteins, some are calling for a re-evaluation of decontamination procedures for surgical instruments. Furthermore, since all subjects died before displaying any actual symptoms associated with Alzheimer’s, it is not known if they would have developed the condition at all.

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