How an unusual medical procedure transmitted Alzheimer’s

Alzheimer’s disease’s impact is growing as our population ages, but much of the disease’s pathophysiology remains unclear. A study published last year in the journal Nature revealed a significant new finding about Alzheimer’s disease–it could spread between individuals under unusual circumstances. The finding is one of several that link Alzheimer’s to rare prion diseases, a connection that could change how we prevent and treat dementia. 

A dangerous donation

Craniopharyngioma is a benign brain tumor, meaning it isn’t cancerous. However, these small growths, which squat in the base of the brain, still have devastating side effects. They open shop next to the pituitary gland, a source of critical hormones. In adults, this can affect sexual performance or menstrual cycles. 

In children, the tumor can stunt growth in crucial years of life. Biologists found a breakthrough treatment for these children in the 1950s–human growth hormone. Usually released by the pituitary gland, the scientists found that human growth hormone could be extracted from other people and donated to those with craniopharyngioma. Donors could even give their hormones after death. However, over the 25 years that children received these donations, some patients’ lives changed for the worse. 

The problem with the treatment was one missing step. Most of the donation protocols required that clinicians sieve donated brain extract using a technique called size-exclusion chromatography. This separation ensured that large protein aggregates were absent from the final donation. One approach omitted this step, with disastrous consequences. Two hundred children developed Creutzfeldt-Jakob disease (CJD)–a rare prion disease that causes rapid brain damage and dementia. Since the donation protocols had not screened the PrP protein out of the donated samples, some of the patients were sickened. 

In response, the use of cadaver-derived growth hormone was immediately and permanently suspended. But prion diseases can take decades to emerge, so researchers have monitored affected children throughout the rest of their lives. 

That explains why it took until 2024 for scientists to realize that prion disease wasn’t all that had slipped through the net. 

‘Alzheimer’s can be induced’

The 2024 study led by University College London professor John Collinge reported on five growth hormone recipients who had developed Alzheimer’s disease pathology at incredibly young ages–one at just 39 years old. Collinge’s group had previously reported that some of the growth hormone batches that four members of the group received had been contaminated with amyloid beta and tau, two proteins that are heavily implicated in the onset of Alzheimer’s disease.  

Lary Walker, a neurologist and neurodegenerative disease researcher at Emory University, has argued for decades that the way Alzheimer’s disease spreads in the brain mimics the march of prion proteins. Walker explains to Popular Science that colleagues had often received his experimental work with the same hesitancy–that findings in animal models may not be replicable in humans. This new study shows that these findings are replicable, according to Walker. The paper “indicates that actual Alzheimer’s disease can be induced in all of its manifestations in humans,” Walker added. 

Richard Knight, a prion researcher at the University of Edinburgh, explains that prion diseases and other neurodegenerative conditions are linked by shared mechanisms. “They all involve the deposition of an abnormally folded normal protein in the tissue,” Knight tells Popular Science. The conditions also usually all begin in one specific brain area and spread. 

But prion diseases differ from other conditions in their aggressiveness. Knight, who worked in the field during the outbreaks of CJD that affected the UK in the 1990s, points out that the disease can progress at a terrifying rate. CJD could begin in the cerebellum, affecting coordination, but then affect the whole brain in weeks. “Alzheimer’s disease might spread over a decade or more,” Knight explains. 

Transmission and transfusion 

Knight says that the method of transmission that Collinge identified is “extremely unusual,” and there’s no evidence that Alzheimer’s can spread through medical procedures used today. He also conceded that if Alzheimer’s could spread more easily, it would be much harder to notice. 

An exploratory 2023 study published in the journal JAMA Internal Medicine raised the troubling prospect that blood transfusions could possibly transmit the amyloid-linked disease cerebral amyloid angiopathy (CAA). Prion diseases like CJD may also be spread via blood transfusions. The study authors wrote that their results require replication to interpret correctly, but it would be hard to determine if either CAA or Alzheimer’s disease, can be transmitted this way.

Prion disease is incredibly rare. Knight explains that when several blood donors and their recipients both went on to develop prion disease, it quickly became apparent that it was no coincidence. But when 40 percent of people over age 90 have dementia, it becomes much more challenging to work out which cases may have been transmitted via blood, a patient’s genetics, or environmental factors. 

Exploring how disease-causing proteins spread is essential work, which could help improve treatments by pointing researchers toward early biomarkers of disease. Understanding these proteins could also answer pressing questions about risk factors for these conditions. While Alzheimer’s isn’t infectious like diseases from a virus or bacteria, establishing how this disease moves can help us stop it altogether in the future.  

 

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