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Dr. Leslie Norins is willing to pay a million dollars of his own money to anyone who can clarify: Alzheimer's disease, the most common form of dementia in the world, is caused by a germ?
By "germ" it means 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 many an easy way to drain one's research budget from superimposed science. Money has been investing for years in Alzheimer's research, but until recently, little of this money was spent researching an infectious cause of dementia.
But this "germ theory" of Alzheimer's disease, as Norins calls it, has been fermenting in the literature for decades. Even the early twentieth-century Czech physician, Oskar Fischer – who, with his German contemporary, Dr. Alois Alzheimer, played a pivotal role in describing the disease – pointed to a possible link between newly identified dementia and tuberculosis. .
If the germ theory is gaining ground, if only for a subgroup of Alzheimer's patients, it could trigger a dramatic change in the way doctors understand and treat the disease.
For example, would we see a day when dementia is prevented with a vaccine or treated with antibiotics and antiviral drugs? Norins thinks this deserves to be studied.
Norins earned his medical degree from Duke in the early 1960s and, after a stint at the Centers for Disease Control and Prevention, he began a lucrative career in medical publishing. He eventually settled in a relatively old community in Naples, Florida, where he became interested in dementia and began reading about it.
After going through the medical literature, he noticed a pattern.
"It appeared that many of the reported features of Alzheimer's disease were consistent with an infectious process," Norins told NPR. "I thought for sure that it had already been studied because millions and millions of dollars were spent on Alzheimer's research."
But apart 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 disease's germ theory. Alzheimer's, and through which its price will be distributed. A white paper that he wrote for the site reads as follows: "After a review of the scientific literature carried out for two years, it is now clear that only one germ – the only one in the world. identity not yet specified, and perhaps not yet discovered – causes the essence of the disease – calling it the "Alzheimer's germ."
Norins is reluctant to cite sources and studies supporting his claim, including a 2010 study published in the Journal of Neurosurgery[1] showing that neurosurgeons die of Alzheimer's disease at a rate nearly 2.5 times higher than that of the general population.
Another study of the same year, published in the Journal of the American Geriatric Society,[2] found that people with spouses with dementia were 1.6 times more likely to develop the disease.
The contagion comes to 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[3] calling for "further research on the role of infectious agents in [Alzheimer’s] causality. "Based on most of the evidence that Norins has encountered, the authors concluded that clinical trials on antimicrobial drugs used in Alzheimer's disease were now warranted.
An intriguing study published in neuron[4] in July suggests that viral infection can affect the progression of Alzheimer's disease. Led by Joel Dudley, a professor of genetics at Mount Sinai, the work aimed to compare the genomes of healthy brain tissue to those with dementia.
But something was not stopping: herpes.
The Dudley team has found an exceptionally high viral DNA level derived from two human herpes viruses, HHV-6 and HHV-7. Viruses are common and cause a rash called roseola in young children (and not the sexually transmitted disease caused by other strains).
Some viruses have the ability to remain dormant in our neurons for decades by incorporating their genome into ours. The classic example is that of chickenpox: an infant viral infection resorbs and hides silently, returning years later as a shingles, an excruciating rash. Like it or not, we are almost all chimeras with viral DNA staining our genomes.
But the only herpes virus does not mean an inevitable decline of the brain. After all, up to 75% of us can host the HHV-6.[5]
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 influences at the origin of the disease – a combination that causes what some consider to be the major factor of the disease, an immune system hyperactive.
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 root cause of Alzheimer's disease is drying up. But protein can still contribute to the disease, even if it ends up being considered infectious.
Works of Rudolph Tanzi, neuroscientist at Harvard[6] suggests that it could be a bit of both. Along with his colleague Robert Moir, Tanzi showed that amyloid was deadly for viruses and bacteria in the test tube as well as in the mouse. 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 the amyloid reaction is harmless? According to Tanzi, it is not so simple.
Tanzi think that in many cases of Alzheimer's, microbes are probably the initial seed that triggers a toxic tumble of molecular dominos. At the beginning of the pathological process, the amyloid protein accumulates to fight the infection, but too much of the protein begins to alter the functioning of neurons in the brain. The excess amyloid then causes the entanglement of another protein, the tau protein, which is more harmful to brain cells.
But, as Tanzi explains, the ultimate reaction of the body to this neurotoxic disorder is the ultimate neurological insult of Alzheimer's disease. All excess protein strengthens the immune system, causing inflammation – and it is this inflammation that causes the most damage to the brain with Alzheimer's disease.
What does this say about the future of treatment? Maybe a lot. Tanzi envisions a day when people go to screening, say, at age 50. "If their brain is stuffed with too much amyloid," he says, "we're tackling it a bit with antiviral drugs – it's like if you're prescribing preventative medications if your cholesterol is too high. "
Tanzi believes that microbes are just one of the possible seeds of the complex pathology that causes Alzheimer's disease. Genetics can also play a role because some genes produce a type of amyloid that is more likely to clump together. He also believes that environmental factors such as pollution could contribute to this.
Dr. James Burke, professor of medicine and psychiatry at the Alzheimer's Disease Research Center at Duke University, does not wish to give up the theory of amyloid, but agrees that the time came to the field to move on. "The development of Alzheimer's disease can take many ways and it would be difficult to focus solely on amyloid and tau," he said. "A million dollar prize draws attention, but the reward of identifying a treatable target to delay or prevent 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 targeting amyloid. But the included patients may have been too advanced in their illness to benefit therapeutically.
If a microbe is responsible for all or some of the Alzheimer's cases, future treatments or preventive approaches may help prevent the accumulation of toxin-containing proteins. Tanzi and Norins both believe that vaccines against Alzheimer's disease may one day become common practice.
Last July, in collaboration with Norins, the Infectious Diseases Society of America announced plans to offer two $ 50,000 grants to research on a microbial association with Alzheimer's disease. According to Norins, this is the first recognition by a large group of infectious diseases that Alzheimer's disease can be microbial in nature – or at least that it deserves to be explored.
"The important thing is not the amount of money, which is paltry compared to the $ 2 billion spent by the NIH for research on amyloid and tau," says Norins. , "Remember when we thought that ulcers were caused by stress?"
We now know that ulcers are caused by a germ.
This article appeared originally on Shots, NPR's health blog.
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