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Dr. Leslie Norins is ready to hand over a million dollars of his own money to anyone who can clarify something: Alzheimer's disease, the most common form of dementia in the world, is it caused by a germ?
By "germ" it refers to microbes such as bacteria, viruses, fungi and parasites. In other words, Norins, a doctor turned publisher, wants to know if Alzheimer's disease is contagious.
It's an idea that, just a few years ago, would have seemed to be a simple way to drain your superimposed science research budget. The money has been invested in research on Alzheimer's disease for years, but until very recently, little has been spent on the infection caused by dementia.
But this "germ theory" of Alzheimer's disease, as the Norins call it, has been fermenting in the literature for decades. Even the Czech physician Oskar Fischer, at the beginning of the 20th century, who, with his German contemporary Alois Alzheimer, was the first to describe the disease, spoke of a possible link between newly identified dementia and tuberculosis.
If the germ theory is gaining momentum, even in some patients with Alzheimer's disease, this could trigger a seismic shift in the way doctors understand and treat the disease.
For example, will we see a day when dementia is prevented with a vaccine or treated with antibiotics and antiviral drugs? Norins thinks it's worth watching.
Norins received his medical degree from Duke in the early 1960s and, after a stint in the Centers for Disease Control and Prevention, began a lucrative career in medical publishing. He eventually settled in a certainly elderly community of Naples, Florida, where he became interested in dementia and began reading the situation.
After going through the medical literature, he noticed a pattern.
"It turned out that many of the features of Alzheimer's disease reported were consistent with an infectious process," Norins told NPR. "I thought it had to be studied already, because millions and millions of dollars were spent on Alzheimer's disease research."
But aside from the scattered interest over the decades, this was not the case.
In 2017, Norins launched Alzheimer's Germ Quest, Inc., a public interest company that, he hopes, will spark interest in the germ theory of Alzheimer's disease and through which its price will be distributed. A white paper that he wrote for the site reads as follows: "After a two-year review of the scientific literature, I believe that it is now clear that only one germ – the identity not yet specified, and perhaps not yet discovered – is at the origin of the MA. calling it the "Alzheimer's germ". "
Norins is reluctant to cite sources and studies in support of his request, including a study published in 2010 in the US. Journal of Neurosurgery showing that neurosurgeons die of Alzheimer's disease at a rate seven times higher than for other disorders.
Another study of the same year, published in The Journal of the American Geriatric Society found that people whose spouses have dementia are at six times higher risk for the disease themselves.
The contagion comes to my mind. And Norins is not alone in his thinking.
In 2016, 32 researchers from universities around the world signed an editorial in the Diary of Alzheimer's disease calling for "further research on the role of infectious agents in [Alzheimer’s] causality. "Based on most of the same Norins evidence encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer's disease are now warranted.
NPR has published an intriguing study published in neuron in June, this suggests that viral infection can influence the progression of Alzheimer's disease. Led by Mt. Sinai Genetics Professor Joel Dudley aimed to compare the genomes of healthy brain tissue with those affected by dementia.
But something continued to hinder: herpes.
The Dudley team has noticed a surprisingly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. Viruses are common and cause a rash called roseola in young children (not sexually transmitted diseases caused by other strains).
Some viruses have the ability to remain dormant in our neurons for decades by incorporating their genomes into ours. The classic example is chickenpox: an infant viral infection disappears and hides silently, returning only years later as shingles, an unbearable skin rash. Like it or not, we are almost all viral DNA chimeras that stain our genomes.
But having the herpes virus alone does not mean an inevitable decline of the brain. After all, up to 75% of us could host the HHV-6.
But Dudley also noticed that herpes seemed to interact with known human genes to increase the risk of Alzheimer's. Perhaps, he says, there is a toxic combination of genetic and infectious influence that drives the disease; a combination that causes what some people feel is the main contributor to the disease, a hyperactive immune system.
The characteristic pathology of Alzheimer's disease is the accumulation of a protein called amyloid in the brain. Many researchers have assumed that these aggregates, or plaques, are only a byproduct of another process at the heart of the disease. Other scientists believe that the protein itself contributes to the disease one way or another.
The theory that amyloid is the cause of Alzheimer's disease is losing vigor. But the protein can still contribute to the disease, even if it ends up being considered infectious.
The work of Rudolph Tanzi, neuroscientist at Harvard, suggests that it could be a bit of both. With his colleague Robert Moir, Tanzi has shown that amyloid is deadly for viruses and bacteria in the test tube, as well as in mice. He now believes that protein is part of our old immune system which, like antibodies, speeds up its activity to help fight against unwanted insects.
Does this mean that the microbe is the cause of Alzheimer's disease and that amyloid is a harmless reaction? According to Tanzi, it is not so simple.
Tanzi thinks that in many cases of Alzheimer's, microbes are probably the initial seed that triggers a toxic fall in molecular dominos. At the beginning of the disease, the amyloid protein accumulates to fight the infection, but too much protein begins to alter the function of neurons in the brain. The excess of amyloid then causes another protein, called tau, to form entanglements, further harming brain cells.
But as Tanzi explains, the ultimate neurological reaction in Alzheimer's is the body's response to this neurotoxic disorder. Any excess protein increases the immune system, causing inflammation – and it is this inflammation that causes the most damage to the brain reached by Alzheimer's disease.
So what does that say about the future of treatment? Probably a lot. Tanzi envisions a day when people are screened at the age of 50, for example. "If their brains are riddled with too much amyloid," he says, "we knock them out a bit with antiviral drugs, it's like prescribing preventative medications if your cholesterol levels were too high."
Tanzi believes that microbes are just one of the possible seeds of the complex pathology of Alzheimer's disease. Genetics may also play a role because some genes produce a type of amyloid that is more prone to clumping. He also thinks that environmental factors such as pollution could contribute.
Dr. James Burke, professor of medicine and psychiatry at the Center for Research on Alzheimer's Disease of Duke University, is not ready to completely abandon the theory of amyloid but agrees that it is time to go ahead. "There may be a long way to go to develop Alzheimer's disease and it would be unwise to focus solely on amyloid and tau," he says. "A million dollar award is interesting, but the reward for identifying a treatable target for delaying or preventing Alzheimer's disease is invaluable."
Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit a brain at risk. The vast majority of Alzheimer's disease treatment trials have failed, including many patients targeting amyloid. But it may be that the included patients are too far away in their illness for therapeutic benefit.
If a microbe is responsible for all or some cases of Alzheimer's disease, future treatments or preventative approaches may possibly prevent the accumulation of protein in the toxins. Tanzi and Norins believe that vaccines against Alzheimer's disease, such as herpes, might one day become a common practice.
In July of this year, in collaboration with the Norins, the American Society of Infectious Diseases announced its intention to offer two $ 50,000 grants to research a microbial association with Alzheimer's disease. According to Norins, this is the first recognition by a group of leading infectious diseases that Alzheimer's disease could be microbial in nature – or at least deserving of exploration.
"The important thing is not the amount of money, which is a pittance in comparison to the $ 2 billion spent by the NIH for research on amyloid and tau," said Norins. possibility. Remember when we thought that ulcers were caused by stress? "
We now know that ulcers are caused by a germ.
Bret Stetka is a New York-based writer and editorial director at Medscape. His work appeared in Cable, American scientist and on Atlantic.com. He graduated from the Faculty of Medicine at the University of Virginia. He is also on Twitter: @BretStetka.
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