In exceptional cases
Biologists have successfully "infected" a mouse with Alzheimer's disease for the first time
British scientists have successfully "infected" mice with Alzheimer's disease using an extract of growth hormone from the brains of people suffering from this disease. The results of these experiments were presented in the journal Nature (Purro et al., Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone).
"Now we have experimental evidence that the proteins that cause Alzheimer's disease can actually be transmitted from person to person. It is not yet clear what exactly leads to the development of the disease – growth hormone injections or brain surgery, but both need to be taken into account when treating patients," says John Collinge from University College London (in a press release Amyloid pathology transmission in lab mice and historic medical treatments – VM).
It is believed that Alzheimer's disease is caused by the accumulation of a pathogenic substance inside neurons, the beta-amyloid protein. It is formed from the "scraps" of the APP protein, which is involved in the processes of repairing damaged neurons and forming connections between them. Violations in the processing of molecules of this protein lead to the appearance of plaques and the destruction of nerve cells.
In September 2015, British doctors discovered, studying the brains of people who died from mad cow disease, that Alzheimer's disease can be transmitted from person to person as a result of "infection" of their nervous tissue with foreign proteins. In this case, their source was an extract of growth hormone extracted from the brains of sick donors.
This for the first time put doctors before the fact that Alzheimer's disease can be contagious. The carrier and source of prions, as scientists discovered two years ago, may be some pathogenic bacteria. On the other hand, many scientists doubted the discoveries of their British colleagues, considering the patterns they found to be a coincidence.
Colling and his colleagues answered many of the critics' questions. To do this, they obtained several old ampoules with growth hormone that caused mad cow disease in their patients, and analyzed their chemical composition.
As it turned out, in all these samples there were not only prions that cause mad cow disease, but also beta-amyloid "blanks" consisting of several single protein "scraps", as well as tau protein, another trace of the development of Alzheimer's disease.
After confirming their presence, the scientists tested what would happen if this growth hormone was injected into the body or brain of transgenic mice whose APP gene had been replaced with its human version. As these experiments showed, all rodents were "infected" with Alzheimer's disease.
In particular, after a few months, accumulations of beta-amyloid began to appear in the blood vessels of their brain, and neurons began to show the first signs of degeneration.
Nothing like this, according to Kolling and his colleagues, did not occur in the nervous tissue of mice from the control group who received injections of synthetic growth hormone or "pure" extracts from the pituitary gland.
A section of the brain of mice injected with synthesized growth hormone (a-c) and hormone from old ampoules containing beta-amyloid (d-f). There is a noticeable accumulation of beta-amyloid in the vessels (e versus b) and in the cerebral cortex (f versus c). A drawing from an article in Nature – VM.
Not all critics are happy with such verification of their claims. For example, Professor Roger Morris from King's College London (UK) is skeptical about the new experiences of his colleagues.
According to him, they "did not detect visible traces of amyloid plaques and tau protein in the nerve cells themselves, and used mice initially predisposed to the development of Alzheimer's disease."
"It is extremely important to understand that we are not saying that you can get Alzheimer's disease or mad cow disease by touching a sick person or otherwise contacting him. We are just saying that this problem should be studied in detail," concludes Colling.
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