Color computed tomography scan of a brain affected by Alzheimer’s disease.Credit: Zephyr/Science Photo Library
Researchers say they have found further evidence supporting the controversial hypothesis that a sticky protein characteristic of Alzheimer’s disease can be “transmitted” from person to person through certain surgical procedures. .
The authors and other scientists stress that the study was based on a small number of people and related to a medical practice that is no longer practiced. This study does not suggest that dementias such as Alzheimer’s disease can be contagious.
Still, “we want to continue to take precautions to reduce the occurrence of these rare cases,” said John Collinge, a neurologist at University College London who led the study.1 in natural medicine January 29th.
For the past decade, Collinge and his team have studied people in the UK who were given growth hormone from the cadaveric pituitary gland to treat conditions such as short stature as infants. A new study found that some of these people developed signs of early-onset dementia decades later. Symptoms of dementia, such as memory and language problems, were diagnosed clinically, and some patients developed plaques of the sticky protein amyloid beta, a hallmark of Alzheimer’s disease, in their brains. The authors suggest that this amyloid protein, which was present in the hormone preparation, may have been “seeded” into the brain and caused the damage.
contaminated hormones
The study builds on the team’s previous work on people who were given cadaver-derived growth hormone, a practice that the UK discontinued in 1985. In 2015, the Collinge team stated:2 Amyloid beta deposits were found in the postmortem brains of four people treated with growth hormone. These people had died in middle age from Creutzfeldt-Jakob disease, a fatal neurological disease caused by infectious misfolded proteins called prions. Prions were present in a batch of growth hormone.
The four people analyzed in that study died before clinical symptoms associated with amyloid accumulation were observed. However, the presence of these amyloid plaques within blood vessels in the brain suggested that they had developed a condition called cerebral amyloid angiopathy (CAA). CAA causes bleeding in the brain, which is often a precursor to Alzheimer’s disease.
Collinge’s team also located and studied archived batches of cadaver-derived growth hormone. In the 2018 survey2They discovered that the hormone preparation contained amyloid beta protein, and when injected into mice, this preparation caused the development of amyloid plaques, causing CAA in the animals.
This led the research team to believe that the contaminated hormones may have led to the development of Alzheimer’s disease in the people who received them. In Alzheimer’s disease, amyloid plaques within brain tissue are thought to cause loss of neurons and brain tissue.
New research shows that 5 out of 8 people who received hormone therapy in childhood but did not develop Creutzfeldt-Jakob disease developed behavioral signs of early-onset dementia later in life, between the ages of 38 and 55. It was discovered that he had developed. Collinge’s team claims that these five people, studied through clinics, medical records and brain scans, meet the criteria for a diagnosis of early-onset Alzheimer’s disease.
genetic testing
Early-onset Alzheimer’s disease is usually caused by specific genetic mutations, but researchers found that three of the people who showed signs of Alzheimer’s disease and had DNA samples available for testing had these mutations. Couldn’t find it. “This is consistent with these patients developing some type of Alzheimer’s disease as a result of childhood treatment with this contaminated pituitary hormone,” Collinge says. The authors jointly claim that their study suggests that in rare cases, Alzheimer’s disease may be transmitted through transmissible biological agents.
Tara Spiers-Jones, a neuroscientist at the UK Dementia Research Institute at the University of Edinburgh, UK, said the small size of the study limited the strength of the results. “Are the amyloid-beta species from hormone therapy involved in the development of dementia? It’s hard to know with just eight of us,” she says.
Matthias Uecker, a neuroscientist at the German Center for Neurodegenerative Diseases in Göttingen, points out that people could have developed dementia regardless of hormone treatment. “These people had a variety of medical conditions that may have increased their risk of developing neurodegenerative diseases like Alzheimer’s disease,” he says.
Researchers including Spiers-Jones also question whether people with dementia actually had Alzheimer’s disease, despite their clinical diagnosis.
Andrew Doig, a neuroscience researcher at the University of Manchester in the UK, agreed: “Errors often occur when diagnosing the type of dementia a person has during their lifetime.”
From a public health perspective, Spiers-Jones says there is no need to worry about “contagious” dementia today. “This treatment no longer exists,” she says.
Despite the study’s limitations, the scientists say the study furthers our understanding of neurodegenerative diseases. “I’m glad that people are doing great research to better understand how amyloid beta disseminates neurodegenerative diseases,” says Spiers-Jones.
“I think many other scientists will be looking for additional evidence to explore the idea of transmissible Alzheimer’s disease,” says Uecker.