New study provides first evidence of environmentally acquired Alzheimer’s disease

By Lisa Marie Basile | Fact-checked by Davi Sherman
Published February 1, 2024

Key Takeaways

  • Research published in Nature describes strange circumstances behind the eight people who developed Alzheimer’s disease (AD) following childhood treatment, suggesting that iatrogenic AD is possible. 

  • The specific treatment involved contaminated samples of cadaver-derived pituitary growth hormone, which is now no longer used as a treatment option.

  • Researchers and clinicians emphasize that the circumstances contributing to the eight AD diagnoses were extraordinary, and that AD cannot be transmitted between people.

New research published in Nature illustrates how Alzheimer’s disease (AD) was transmitted to eight people under extremely specific and rare circumstances.[] 

Extraordinary circumstances for AD transmission

AD affects an estimated 6.7 million Americans, the majority of whom are women and people over 75 years of age. By 2050, the number of people with AD may grow to an estimated 12.7 million.[] 

AD is not a contagious disease, but extraordinary circumstances can lead to its transmission.

In previous research, human transmission of amyloid-beta deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy or CAA) was reported in young adults who had died of Creutzfeldt-Jakob disease (CJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and amyloid-beta seeds.[]

CJD is a rare disorder that affects muscle coordination, thinking, and memory. 

The new research builds on this, describing eight patients—each referred to, or reviewed by, the National Prion Clinic (NPC) between 2017 and 2022—who received c-hGH treatment but did not die.[] These patients “developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms,” the researchers state.

The researchers believe that amyloid-beta is thought to be the root cause of AD, and is found “in the form of parenchymal deposits, including neuritic plaques, and parenchymal and leptomeningeal vascular aggregation, corresponding to CAA. CAA is seen as a co-pathology in the large majority of people with Alzheimer’s disease and can also independently present with intracerebral hemorrhage,” they write.

Building on prior research

Previous experiments substantiated the idea that iatrogenic amyloid-beta transmission had occurred in people treated with c-hGH, according to postmortem reports.  

However, in the eight individuals studied, this is the “first time iatrogenic Alzheimer’s disease has been described,” according to research author and neurologist John Collinge, as quoted in Science News.[] 

A diagnosis of iatrogenic CJD was ruled out for all eight patients—in two cases by postmortem examination. Five of the patients (four out of five of whom experienced symptom onset between the ages of 38 and 49 years) had symptoms consistent with early onset dementia, including progressive cognitive impairment. 

In three of the five patients, an AD diagnosis had already been made prior to the referral to the NPC. Two of these patients presented with typical amnestic issues, while the other three did not. Of the other three patients, one (42 years old at onset) had mild cognitive impairment; one had subjective cognitive symptoms only; and one was asymptomatic but met the ATN classification system criteria for AD. The researchers say that in the patients with symptoms, the latency from c-hGH exposure was 30 to 40 years.

The medical procedure that led to AD

All of the patients described in the research received c-hGH prepared by the Wilhelmi or Hartree-modified Wilhelmi preparation (HWP) method. This suggests, the researchers conclude, that the iatrogenic AD was caused by the HWP method preparation of c-hGH. 

“Although we cannot exclude the possibility that childhood diagnosis and/or its treatment might modify the risk of developing cognitive symptoms, if these childhood diagnoses were alone responsible for the observed findings, we would have expected equivalent referrals of patients who had received only non-HWP c-hGH, which we did not receive,” the authors write.

A 2019 article co-authored by Collinge and published in Nature explained that 80 patients who had developed CJD were treated with c-hGH prepared by the HWP procedure.[] 

Your patients may worry about 'catching' AD

They shouldn't, of course. “Although iatrogenic AD may be rare, and there is no suggestion that [amyloid-beta] can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures,” the researchers said in a piece associated with the research.[] It is likely rooted in the introduction of amyloid-beta in early life.[] 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup—similar to that seen in Alzheimer’s—in the brain of an animal by injecting it with amyloid-beta,” says Christopher Weber, PhD, Director of Global Science Initiatives at Alzheimer’s Association. “We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains. But these things do not happen in daily life or in routine medical procedures.”

“Human growth factor from cadavers is no longer used as a treatment," Dr. Weber continues.

"Since the treatments described in this paper were stopped, we have learned a lot about ensuring that donated samples of all types are treated to avoid any contamination from the donors."

Christopher Weber, PhD

Patients should know that this will not happen to them or to people in their family, Dr. Weber says. “It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of pathogen transmission are eliminated,” he adds.

The bottom line? “We shouldn't put amyloid-beta into people’s brains, either accidentally or on purpose. And appropriate measures should be in place to ensure that doesn’t happen,” Dr. Weber says.  

What this means for you

New research reports on eight patients who developed dementia and biomarker changes associated with Alzheimer's disease (AD) after receiving childhood treatment for Creutzfeldt-Jakob disease (CJD) in the form of contaminated cadaver-derived pituitary growth hormone (c-hGH). The researchers suggest that AD, like CJD, has environmentally acquired forms. The iatrogenic AD in these cases is linked to the HWP method preparation of c-hGH, emphasizing the need to review measures to prevent accidental transmissions in medical procedures.

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