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Infectious theory about Alzheimer's disease benefits from interest

Dr Leslie Norins is willing to hand over $ 1 million of his own money to anyone who can clarify…

Dr Leslie Norins is willing to hand over $ 1 million of his own money to anyone who can clarify something: Is Alzheimer’s disease, the most common form of dementia worldwide, caused by a bacterium?

“germ” means microbes such as bacteria, viruses, fungi and parasites. In other words, Norins, a doctor-edited publisher, wants to know if Alzheimer’s disease is contagious.

It’s an idea that a few years ago would have seemed many easy ways to empty its research budget on bunk science. Money has poured into Alzheimer’s research for years, but until recently, much of it did not go into investigating a contagious cause of dementia.

But this “germ theory” of Alzheimer’s, as Norins calls it, has guessed in literature for decades. Until the beginning of the 20th century, Czech doctor Oskar Fischer-som, together with his German contemporary Dr Alois Alzheimer, was integrated in first describing the condition &#821

1; noted a possible connection between newly identified dementia and tuberculosis.

If the germ theory gets traction, even in a subset of Alzheimer’s patients, it may trigger a seismic shift in how doctors understand and treat the disease.

Ex. Should we see a day when dementia is prevented with a vaccine or treated with antibiotics and antiviral drugs? Norins believes it is worth looking at.

Norins received his medical exam from Duke in the early 1960s, and after a stint at Centers for Disease Control and Prevention, he fell in a lucrative career in medical publishing. He eventually settled in a probably older community in Naples, Florida, where he took interest in dementia and began to read on the condition.

After cutting the medical literature, he noticed a pattern.

“It was found that many of the reported properties of Alzheimer’s disease were consistent with an infectious process,” said Norin’s NPR. “I thought it must have been investigated since millions and millions of dollars have been spent on Alzheimer’s research.”

In 1967, Norins launched Alzheimer’s Germ Quest Inc., a public wealth company he hopes will drive interest in Alzheimer’s nuclear theory, through which his award will be distributed. A white paper He wrote at the site, reads: “From a two-year review of the scientific literature, I think it is clear that only a bacterial identity that has not yet been specified and possibly not yet discovered causes most AD. I’m calling it “Alzheimer’s Germ.” “

Norins is quick to quote sources and studies that support his statement, including a 2010 study published in Journal of Neurochirurgia [1] showing that neurosurgery dies of Alzheimer’s almost 2.5 times higher than for that

Another study from the same year published in the Journal of the American Geriatric Society, [2] found that persons whose spouses have dementia are 1.6 times greater risk of the condition itself.

Infected occurs. Norins is not alone in his thinking.

In 2016, 32 researchers from universities around the world wrote an editorial in the Journal of Alzheimer’s Disease [3] who requested “further research on the role of contagious agent in [Alzheimer’s] causal relationship. “Based on much of the same evidence as Norins encountered, the authors found that clinical trials with antimicrobial drugs in Alzheimer’s are now justified.

An exciting study published in Neuron [4] in July indicates that viral infection can affect The development of Alzheimer’s led by Mount Sinai Genetics Professor Joel Dudley, whose work was intended to compare the genes of healthy brain tissue with those who suffered from dementia.

But something continued to get in the way: herpes.

Dudley’s team noticed an unexpected high level of viral DNA from two human herpesviruses, HHV-6 and HHV-7. The viruses are common and cause rashes called roseola in young children (not the sexually transmitted disease caused by other strains.)

Some viruses have the ability to remain dormant in our nervous cells for decades by integrating their genomes into our own. The classic example is chickenpox: a childhood virus infection l looking and lurking quietly, returning years later as shingles, a rash eradication. Like it or not, almost all of us are chimeras with viral DNA that speckle our genomes.

But with the herpes virus alone, it does not spell inevitable brain failure. After all, up to 75% of us can have HHV-6. [5]

However, Dudley also noted that herpes seemed to interact with human genes known to increase Alzheimer’s risk. Perhaps, he says, there is a certain toxic combination of genetic and infectious influence that leads to the disease – a combination that rumors what some feel is the main contributor to the disease, an overactive immune system.

Alzheimer’s distinctive patology is the accumulation of a protein called amyloid in the brain. Many researchers have assumed that these aggregates or plaques are simply a byproduct of any other process at the core of the disease. Other scientists believe that the protein itself contributes to the state in some way.

The theory that amyloid is the basis for Alzheimer’s is to lose steam. But the protein can still contribute to the disease, even if it blows up as infectious.

The work of neuroscience Rudolph Tanzi [6] by Harvard indicates that there may be a bit of both. Together with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube and also in mice. He now believes that the protein is part of our old immune system, which, as antibodies, frames up its activity to help remedy unwanted bugs.

Does that mean that the microbe is the cause of Alzheimer’s and Amyloid’s harmless reaction to it? According to Tanzi, it is not that easy.

Tanzi believes that in many cases of Alzheimer’s, microbes are probably the original seed that resigns from a toxic tumor of molecular dominoes. Early in the disease process, amyloid protein builds up to fight infection, but too much of the protein begins to weaken the function of neurons in the brain. The excess amyloid then causes another protein, rope, to form stains, further damaging brain cells.

However, as Tanzi explains, the ultimate neurological insult is in the Alzheimer’s body’s response to this neurotoxic mess. All excess protein increases the immune system and causes inflammation – and this is the inflammation that is most harmful to Alzheimer’s affected brain.

What does this say about the future of treatment? Possibly a lot. Tanzi represents a day when people are screened, say 50 years old. “If their brains are riddled with too much amyloid,” he says, “we’re doing a bit of antiviral medication. It’s just like how you prescribe preventive drugs if your cholesterol is too high.”

Tanzi believes that microbes are just a possible seed for the complex pathology behind Alzheimer’s. Genetics can also play a role, as some genes produce a type of amyloid more prone to clumping. He also feels that environmental factors such as pollution can contribute.

Dr James Burke, professor of medicine and psychiatry at Duke University’s Alzheimer’s Disease Research Center, is not willing to abandon the amyloid theory, but agrees that it’s time for the field to move on. “There may be many ways to develop Alzheimer’s disease, and it would be brief to focus only on amyloid and rope,” he says. “One million dollar price is attention, but the reward for identifying a treatable goal of delaying or preventing Alzheimer’s disease is invaluable.”

Any treatment that interferes with the cascade that leads to amyloid, tau and inflammation can theoretically benefit a risk to the brain. The vast majority of Alzheimer’s treatment trials have failed, including many targeted amyloids. But it may be that the included patients were too far in their disease to harvest any therapeutic benefit.

If a microbial is responsible for all or some cases of Alzheimer’s, future treatments or preventive methods may prevent the development of toxin protein in the first place. Both Tanzi and Norins believe that Alzheimer’s vaccine against viruses like herpes may become commonplace one day. [July19659016] In July this year, the Infectious Diseases Society of America announced that it plans to offer two $ 50,000 contributions to support research into a microbial association with Alzheimer’s. According to Norins, this is the first confirmation of a leading infectious disease group as Alzheimer’s may be microbial in nature – or at least it’s worth exploring.

“The important thing is not the sum of money, which is a pittance compared to the $ 2 billion that NIH spends on amyloid and rope research,” says Norins, “but rather respectability and the more general status of scholarships to investigate the infectious possibility. Remember, when we thought that wounds were caused by stress? “

Wounds we know now are caused by a bacterium.

! This article originally appeared on Shots, NPR’s Health Blog.

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