On December 13th, a research team from the UK published a paper in Nature , announcing that they found that β-amyloid causing Alzheimer's disease can metastasize between groups under specific conditions , and in the brain of “infected” Cause new damage. Although this study does not indicate that Alzheimer's disease is widely contagious, β-amyloid may still be transmitted between humans through medical procedures such as surgery and cause brain diseases in a few decades.
As early as 2015, the British team John Collinge team wrote in Nature that they "discovered" evidence that Alzheimer's disease (AD, often called Alzheimer's) can be transmitted.
Recently, the John Collinge team again issued a document confirming that the β-amyloid pathology causing Alzheimer's disease can be transmitted interpersonally through improper medical procedures .
In fact, John Collinge is only an expert in the study of prions. Why is he concerned about the AD field?
This is to start with a famous case in history.
a tragedy
In the 1950s, it was discovered that the application of "growth hormone (GH)" can help people with short stature to raise their height. Scientists have tried to separate and purify growth hormone from animals and humans. Growth hormone extracted from the pituitary gland of human cadaver became the first growth hormone for therapeutic use, known as cadaveric human growth hormone (c-hGH) .
Since 1958, the United Kingdom has treated 1,848 short-skinned people with cadaveric human growth hormone. Unfortunately, some people who received the injection suffered from the deadly disease Creutzfeldt–Jakob disease, a human prion disease characterized by a misfolding and accumulation of brain proteins called “prion proteins”. Sexual, irreversible brain damage).
The incubation period of Keya disease is about 5 to 40 years. Later, at least 200 patients who had been treated with c-hGH in childhood were found to have Creutzfeldt-Jakob disease.
The corpse-derived human growth hormone contaminated with prions caused the spread of Creutzfeldt-Jakob disease in medical treatment. After this was discovered, c-hGH treatment was quickly stopped, which also contributed to the synthesis of recombinant human growth hormone (rhGH). ) Become the standard treatment.
Unexpected discovery
Unexpectedly, in 2015, John Collinge, who focused on prion research, examined the pathological features of β-amyloid in their brains during autopsy patients with Keya disease! It is well known that abnormal accumulation of β-amyloid in the brain is an important pathological feature of AD and cerebral amyloid angiopathy (CAA).
However, these Kayah's dead are still young, only 36 to 51 years old. It is rare for this age group to have AD, and these patients also have no genetic mutations in the early-type AD. So, where are the pathological features of β-amyloid in the brains of these patients?
This discovery by John Collinge in 2015 seems to indicate that the patient developed a beta-amyloid condition due to c-hGH therapy, that is, the pituitary gland used to produce cadaveric human growth hormone actually contains beta-starch. The "seed" of the protein, which causes the patient to be "infected" by the pathological phenomenon.
This is a big event and must be further proven.
Model test
In a study published on December 13, to test whether beta-amyloid in these batches could cause amyloid pathology, the John Collinge team injected samples directly into the brains of model mice.
The results showed that after 240 days of injection, these mice produced beta-amyloid deposits and cerebral amyloid angiopathy, which were similar to those of the deceased. However, almost all of the control mice (including the mice injected with the currently used synthetic recombinant hGH) did not appear at all.
Tau protein is another pathogenesis of neurodegenerative diseases such as AD. Next, the researchers tried to prove whether the protein also has a "seed"-like spread potential like beta-amyloid.
Surgical significance
In summary, the above findings demonstrate that the original batch of c-hGH contains β-amyloid seed, which can be used to sow β-amyloid pathology in mice, and provides experimental evidence to support the hypothesis: β-starch Protein-like pathology can be transmitted interpersonally through iatrogenic methods.
However, there is no need to be overly flustered. The authors emphasize that this study does not mean that Alzheimer's disease is an infectious disease or can be transmitted through blood transfusion, but they believe that assessing the risk of iatrogenic transmission of amyloid pathology is of great significance. .
Another researcher suggested that in order to minimize the iatrogenic infection, all medical supplies should be applied once or strictly. Diseases caused by irregular use of medical supplies are the most painful lessons of history, such as viral infections (HIV, hepatitis B virus, etc.), infectious protein factors (prion).
Paper link:
Https://www.nature.com/articles/s41586-018-0790-y
Reference materials:
'Transmissible' Alzheimer's theory gains traction
Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone
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