One doctor believes it may be possible, and he’s offering a million dollars to any researcher who produces persuasive evidence in the next three years.

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Could the way we treat Alzheimer’s change dramatically in the near future? Getty Images

Scientists are scrambling to find the mysterious source of Alzheimer’s disease (AD). But what if it’s not that mysterious? What if it’s caused by a germ?

That’s what infectious disease specialist Dr. Leslie Norins can’t stop wondering — so much so that he’s created a public benefit corporation, Alzheimer’s Germ Quest Inc. (AGQ).

The organization is offering any researcher who produces persuasive evidence of an AD “bug” an eye-popping $1 million challenge award.

“I’m not ‘guessing’ that AD iscaused by a germ,” Norins clarified. “I am only saying it might be, and there is so much death and suffering at stake that we need to find out, one way or another.”

According to the Alzheimer’s Association, 5.7 million Americans are currently living with AD.

Every 65 seconds, another devastating diagnosis is made and by mid-century, the condition is expected to become even more common: Someone will learn they have AD every 33 seconds.

It’s an unforgiving condition, one which slowly dismantles both thinking and memory. And so far, there’s no way to prevent AD, cure it, or even permanently slow the progression of its symptoms.

The disease was first discovered in 1906, when Dr. Alois Alzheimer discovered shrunken nerve cells in the postmortem brain of a patient who had suffered from memory loss. Still, awareness of the condition didn’t begin in earnest until the 1980s.

In the decades since, scientists have made some key discoveries — that there’s a genetic component, for instance, and lifestyle factors like a healthy diet, regular exercise, and an active social life may offer some protection.

Yet the root cause (or causes) of AD remain elusive.

The most popular theory is still “plaques and tangles.”

Beta-amyloid is a protein that’s broken down and flushed out in healthy brains. But in people with AD, this protein hardens into a plaque that prevents the brain’s nerve cells from working like they should.

Also gumming up the works are fibers of another protein called tau, which transport nutrients between brain cells. In people with AD, they’re inexplicably tangled.

What isn’t understood yet is what causes these plaques and tangles in the first place. Obesity? Head trauma? Silent strokes? High blood pressure? A family history of dementia? Advancing age? These are all considered risk factors for AD.

“There are many potential provocative and causative factors involved in AD, which makes this disease difficult to solve and understand,” said Dr. Verna R. Porter, a neurologist and director of programs for dementia, Alzheimer’s disease, and neurocognitive disorders at Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, California.

Norins never planned to take such an acute interest in AD. A graduate of Johns Hopkins University and Duke Medical School, he studied immunology in Australia before directing a laboratory at the Centers for Disease Control and Prevention. He also spent over 40 years as a medical newsletter publisher.

But the city where he resides, Naples, Florida, is filled with retirees, and over the years, Norins began learning of more — and more — people with AD diagnoses.

“Purely from medical curiosity, I thought I should update myself on this ailment, which I had not really thought about since 50 years earlier in med school,” Norins said.

Given his background with infectious diseases, he wondered if a germ might play a role, but was “flabbergasted” at what he considers a dearth of research, especially when it came to widely testing available antiviral drugs or antibiotics as AD treatments.

Penicillin, for instance, can treat both syphilis and Lyme disease, two infections known to lead to dementia.

“We’ve seen hints in literature for at least a decade that there may be a contribution of some microorganism [to AD], but it’s an area of research that’s been on the fringe a little bit,” said Keith Fargo, PhD, director of scientific programs and outreach for the Alzheimer’s Association. “It just hasn’t picked up speed, usually because the study sizes are small or they tend to have mixed results.”

Nine months ago, in an effort to spur both research and interest, Norins decided to create AGQ and his million-dollar reward challenge. So far, 22 researchers from around the world have signed up.

“There truly is nothing to lose,” Norins said.

If AD does turns out to be caused by a microbe or parasite, “we may already have the anti-infective drug against it or can develop one,” he noted. “We might be able to create a vaccine, in the way we now vaccinate adults against shingles, flu, and pneumonia.”

Other experts in the field of AD are thinking along the same lines. After all, other deadly diseases like AIDS, malaria, tuberculosis, and Zika turned out to be caused by germs.

The human genome is “littered with remnants of human viruses,” said Cory Funk, PhD, a senior scientist at the Institute for Systems Biology in Seattle. “On average, each individual [is carrying] 10 to 12 viruses, although they’re not necessarily causing a full-blown infection.”

So far, over 20 genes have been associated with AD, several of which are also involved with the immune system. Over time, then, can an infection “turn on” one of these genes?

“I don’t think there’s evidence that [a virus] can cause AD, but that they can contribute to it,” said Funk.

He and his colleagues recently published a study in the journal Neuron that found strains of the herpes virus in people affected by AD.

A separate study published in Frontiers in Aging Neuroscience observed that patients treated with antiviral drugs for herpes simplex 1 (the kind that causes cold sores) or herpes simplex 2 (the sexually transmitted infection) had less AD in later life, “so at least there’s a clue such early therapy might prevent some cases of AD later on,” said Porter.

Norins is giving scientists three years to gather evidence about a possible AD “bug.” He calls that length of time “the Goldilocks duration.”

“It couldn’t be too short, like six months, as nobody would have had time to assemble their data. It couldn’t be too long, like 20 years, as that’s basically saying we can’t help the current generation of patients,” Norins said. “‘Take the grant money and poke around for the next 5 to 10 years’ is not a philosophy that appeals to me when 303 Americans are dying every day from Alzheimer’s.”

For people who already have a diagnosis — or who are caring for a loved one with AD — three years will still seem like an eternity. In the meantime, researchers continue to pin down a blood test that can identify early signs of the disease.

Drugs that may finally be able to slow down AD symptoms are currently being tested in clinical trials.

“There’s more optimism and excitement today in the field of dementia research than ever before,” Fargo said. “We’re potentially on the cusp of something that will change the game.”

What that might be, though, is anyone’s guess. Yet everyone’s hope is that a cure quickly follows.