There appears to be a very rare possibility of Alzheimer’s disease transmission between individuals. Researchers report in Nature Medicine that five individuals who had tainted growth hormone injections as youngsters went on to acquire Alzheimer’s disease abnormally early.
In a press briefing on January 25, neurologist John Collinge stated that the results mark “the first time iatrogenic Alzheimer’s disease has been described,” alluding to a condition brought on by a medical procedure.
Although that seems concerning, experts quickly point out that Alzheimer’s disease cannot be spread in daily situations, such as providing care or in the majority of medical settings.
According to Collinge of the Institute of Prion Diseases at University College London, “We are not suggesting for a moment that you can catch Alzheimer’s disease.” “This is not communicable in the sense of an infection caused by bacteria or viruses.”
Neurobiologist Carlo Condello of the University of California, San Francisco, who was not involved in the study, agrees. He states, “We do not consider sporadic Alzheimer’s disease to be a communicable disease in any way.” This is only occurring under highly fabricated, antiquated medical procedures. It is no longer a problem.
In older adults, Alzheimer’s disease typically develops on its own; in the US, for example, 1 in 9 persons 65 and older have the illness. This is one of the peculiarities of these recently reported Alzheimer’s patients. These five patients, who ranged in age from 38 to 55, all had early-onset symptoms. Of those three, for whom genetic information was available, the existence of mutations known to cause early-onset versions of the disease was ruled out by the researchers.
All of the study participants had growth hormone injections when they were younger. These hormones, which were formerly used to treat a variety of growth problems, were taken out of cadavers’ pituitary glands and mixed into batches. Later research revealed that some of these mixes contained contagious prions and malformed proteins that can cause the illness known as Creutzfeldt-Jakob disease. Over 200 persons were impacted worldwide. Since its discontinuation in 1985, doctors have been using synthetic versions of growth hormone therapy.
As it happens, those batches had an additional issue. Four CJD patients’ brains exhibited higher-than-expected levels of amyloid-beta in them, according to a previous study by Collinge and colleagues. Alzheimer’s disease is characterised by the accumulation of sticky proteins, which in these situations is an alarming indication that some of these proteins may have been transferred from donors along with prions (SN: 9/9/15). Researchers found in 2018 (SN: 12/13/18) that A-beta from some of the hormone batches might spread in mice’s brains, indicating that the protein functions something like an infectious prion.
Eight additional patients who were sent to the researchers’ clinical team after receiving growth hormone that was tainted are now included in the study. While none of these individuals had CJD, three had previously been diagnosed with Alzheimer’s. Additional testing revealed that two more patients had the condition and two more had cognitive impairments. One individual exhibited no symptoms.
The researchers conclude that the unexpected introduction of A-beta early in infancy appears to be the most likely cause of these Alzheimer’s patients. According to UCL neurologist Gargi Banerjee, “when taken as a whole, the only real explanation is the shared exposure” to tainted growth hormone, he stated in the briefing on January 25.
Condello states that the view “is plausible.” “What they say it did could have been accomplished by what’s in those extracts.”
However, researchers cannot be positive that these people’s Alzheimer’s disease was brought on by tainted growth hormones. For example, early Alzheimer’s or cognitive issues were likely influenced by the underlying childhood illnesses that required growth hormone therapy, or other medical procedures like radiation. Seizures affected several individuals, which may have contributed to brain damage or cognitive issues. Condello notes that “the definitive answer may never come.”
Beyond these exceptional cases, the findings could provide insight into the mechanisms by which Alzheimer’s disease can develop in the brain and whether A-beta can induce other forms of A-beta to misfold, akin to how prion disease works. Deciphering the specifics of how different A-beta spread variants “lies ahead,” according to Collinge. “A significant amount more research is required.”